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Готові списки джерел за темами / MET/HGF / Статті в журналах

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Статті в журналах з теми "MET/HGF"

Автор: Grafiati

Опубліковано: 15 червня 2024

Оновлено: 31 липня 2025

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1

Toiyama, Y., K. Tanaka, H. Yasuda, et al. "Use of co-expression of HGF and c-Met to predict peritoneal dissemination established by autocrine HGF/c-Met signaling in gastric cancer." Journal of Clinical Oncology 29, no. 4_suppl (2011): 40. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.40.

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40 Background: Epithelial mesencymal transition (EMT) promotes facilitates migration and invasion of epithelial tumour cells. EMT is induced by growth factors implicated in theses process such as hepatocyte growth factor (HGF). Our aim of this study is whether HGF/c-Met pathway is associated with metastasis of gastric cancer (GC), especially in peritoneal dissemination (PD). Methods: HGF and c-Met expression and EMT related molecules were evaluated using real-time PCR and immunohistochemistry in GC tissues. The role of HGF/c-Met pathway for EMT and anoikis was determined and c-Met TKI (SU11274

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2

Zhang, Hongli, Qingqing Feng, Wei-Dong Chen, and Yan-Dong Wang. "HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers." International Journal of Molecular Sciences 19, no. 11 (2018): 3295. http://dx.doi.org/10.3390/ijms19113295.

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The HGF/c-MET pathway is active in the development of digestive system cancers, indicating that inhibition of HGF/c-MET signaling may have therapeutic potential. Various HGF/c-MET signaling inhibitors, mainly c-MET inhibitors, have been tested in clinical trials. The observed efficacy and adverse events of some c-MET inhibitors were not very suitable for treating digestive system cancers. The development of new HGF/c-MET inhibitors in preclinical studies may bring promising treatments and synergistic combination (traditional anticancer drugs and c-MET inhibitors) strategies provided anacceptab

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3

Weimar, Iris S., Daphne de Jong, Egbert J. Muller та ін. "Hepatocyte Growth Factor/Scatter Factor Promotes Adhesion of Lymphoma Cells to Extracellular Matrix Molecules Via α4β1 and α5β1 Integrins". Blood 89, № 3 (1997): 990–1000. http://dx.doi.org/10.1182/blood.v89.3.990.

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Abstract Hepatocyte growth factor (HGF )/scatter factor (SF ) is the ligand for a tyrosine kinase cell surface receptor encoded by the MET protooncogene (c-MET). HGF/SF can induce proliferation and motility in epithelial cells and promotes invasion of carcinoma cells and NIH3T3 fibroblasts transfected with both HGF/SF and c-MET genes. Our results show that HGF/SF and c-MET also play a role in adhesion and invasion of human lymphoma cells. c-MET mRNA is expressed in hemopoietic cells, such as hemopoietic progenitor cells (CD34+ cells) in bone marrow (BM) and mobilized peripheral blood, immature

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4

Gallo, Simona, Valentina Sala, Stefano Gatti, and Tiziana Crepaldi. "Cellular and molecular mechanisms of HGF/Met in the cardiovascular system." Clinical Science 129, no. 12 (2015): 1173–93. http://dx.doi.org/10.1042/cs20150502.

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Met tyrosine kinase receptor, also known as c-Met, is the HGF (hepatocyte growth factor) receptor. The HGF/Met pathway has a prominent role in cardiovascular remodelling after tissue injury. The present review provides a synopsis of the cellular and molecular mechanisms underlying the effects of HGF/Met in the heart and blood vessels. In vivo, HGF/Met function is particularly important for the protection of the heart in response to both acute and chronic insults, including ischaemic injury and doxorubicin-induced cardiotoxicity. Accordingly, conditional deletion of Met in cardiomyocytes result

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5

De Silva, Dinuka M., Arpita Roy, Takashi Kato, et al. "Targeting the hepatocyte growth factor/Met pathway in cancer." Biochemical Society Transactions 45, no. 4 (2017): 855–70. http://dx.doi.org/10.1042/bst20160132.

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Hepatocyte growth factor (HGF)-induced activation of its cell surface receptor, the Met tyrosine kinase, drives mitogenesis, motogenesis and morphogenesis in a wide spectrum of target cell types and embryologic, developmental and homeostatic contexts. Typical paracrine HGF/Met signaling is regulated by HGF activation at target cell surfaces, HGF binding-induced receptor activation, internalization and degradation. Despite these controls, HGF/Met signaling contributes to oncogenesis, tumor angiogenesis and invasiveness, and tumor metastasis in many types of cancer, leading to the rapid growth o

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6

Kauma, Scott, Natalie Hayes, and Shannon Weatherford. "The Differential Expression of Hepatocyte Growth Factor and Met in Human Placenta*." Journal of Clinical Endocrinology & Metabolism 82, no. 3 (1997): 949–54. http://dx.doi.org/10.1210/jcem.82.3.3806.

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Abstract Met is the tyrosine kinase receptor for the ligand hepatocyte growth factor (HGF). Met/HGF plays an important role in epithelial cell proliferation, migration, and morphogenesis. HGF also plays a crucial role in placental development in the mouse. To determine whether HGF potentially has a similar role in human placental development, the production and localization of Met and HGF were determined in early second trimester and term placentas. Reverse transcription-PCR using specific primers demonstrated the expression of Met and HGF messenger ribonucleic acid in placental villi. HGF pro

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7

Yamasaki, Koji, Shoichiro Mukai, Takahiro Nagai, et al. "Matriptase-Induced Phosphorylation of MET is Significantly Associated with Poor Prognosis in Invasive Bladder Cancer; an Immunohistochemical Analysis." International Journal of Molecular Sciences 19, no. 12 (2018): 3708. http://dx.doi.org/10.3390/ijms19123708.

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Hepatocyte growth factor (HGF) plays an important role in cancer progression via phosphorylation of MET (c-met proto-oncogene product, receptor of HGF). HGF-zymogen (pro-HGF) must be processed for activation by HGF activators including matriptase, which is a type II transmembrane serine protease and the most efficient activator. The enzymatic activity is tightly regulated by HGF activator inhibitors (HAIs). Dysregulated pro-HGF activation (with upregulated MET phosphorylation) is reported to promote cancer progression in various cancers. We retrospectively analyzed the expression of matriptase

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8

Woolf, A. S., M. Kolatsi-Joannou, P. Hardman, et al. "Roles of hepatocyte growth factor/scatter factor and the met receptor in the early development of the metanephros." Journal of Cell Biology 128, no. 1 (1995): 171–84. http://dx.doi.org/10.1083/jcb.128.1.171.

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Several lines of evidence suggest that hepatocyte growth factor/scatter factor (HGF/SF), a soluble protein secreted by embryo fibroblasts and several fibroblast lines, may elicit morphogenesis in adjacent epithelial cells. We investigated the role of HGF/SF and its membrane receptor, the product of the c-met protooncogene, in the early development of the metanephric kidney. At the inception of the mouse metanephros at embryonic day 11, HGF/SF was expressed in the mesenchyme, while met was expressed in both the ureteric bud and the mesenchyme, as assessed by reverse transcription PCR, in situ h

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9

Tanaka, Ryota, Mizue Terai, Eric Londin, and Takami Sato. "The Role of HGF/MET Signaling in Metastatic Uveal Melanoma." Cancers 13, no. 21 (2021): 5457. http://dx.doi.org/10.3390/cancers13215457.

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Hepatocyte growth factor (HGF)/mesenchymal-epithelial transition factor (MET) signaling promotes tumorigenesis and tumor progression in various types of cancer, including uveal melanoma (UM). The roles of HGF/MET signaling have been studied in cell survival, proliferation, cell motility, and migration. Furthermore, HGF/MET signaling has emerged as a critical player not only in the tumor itself but also in the tumor microenvironment. Expression of MET is frequently observed in metastatic uveal melanoma and is associated with poor prognosis. It has been reported that HGF/MET signaling pathway ac

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10

Czyz, Malgorzata. "HGF/c-MET Signaling in Melanocytes and Melanoma." International Journal of Molecular Sciences 19, no. 12 (2018): 3844. http://dx.doi.org/10.3390/ijms19123844.

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Hepatocyte growth factor (HGF)/ mesenchymal-epithelial transition factor (c-MET) signaling is involved in complex cellular programs that are important for embryonic development and tissue regeneration, but its activity is also utilized by cancer cells during tumor progression. HGF and c-MET usually mediate heterotypic cell–cell interactions, such as epithelial–mesenchymal, including tumor–stroma interactions. In the skin, dermal fibroblasts are the main source of HGF. The presence of c-MET on keratinocytes is crucial for wound healing in the skin. HGF is not released by normal melanocytes, but

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11

Wu, Xiaxuan, Charitha Marni, Veronica Zhang, et al. "Abstract 2636: Targeting the HGF/MET/TWIST1 pathway in lung adenocarcinoma brain metastases." Cancer Research 85, no. 8_Supplement_1 (2025): 2636. https://doi.org/10.1158/1538-7445.am2025-2636.

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Abstract Lung adenocarcinoma (LUAD) is the most common primary tumor to metastasize to the brain, with ∼40% of patients developing brain metastases (BM) which is associated with poor prognosis. No brain specific targeted therapies currently exist, highlighting the need for novel treatments. We identified a significant enrichment of MET amplification in LUAD BM compared to primary LUAD and liver metastases. MET, a tyrosine kinase receptor, and its ligand hepatocyte growth factor (HGF), mediate proliferation, epithelial-mesenchymal transition (EMT), angiogenesis, and metastasis. We have found th

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12

Kumar, Vinod, Zachary A. Yochum, Princey Devadassan, et al. "Abstract 1091: TWIST1 inhibition overcomes resistance to tyrosine kinase inhibitors in MET driven non-small cell lung cancer." Cancer Research 82, no. 12_Supplement (2022): 1091. http://dx.doi.org/10.1158/1538-7445.am2022-1091.

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Abstract Background: The mesenchymal-epidermal transition (cMET/MET) tyrosine kinase receptor and its ligand, the hepatocyte growth factor (HGF) are overexpressed in a large percentage of non-small cell lung cancers (NSCLCs) and MET mutation and/or amplification leads to oncogene addiction in small subset of NSCLC. In addition, MET amplification is an established mechanism of resistance to EGFR and other oncogenic targeted TKIs. Several MET-inhibitors have been developed and two MET TKIs have been approved for MET exon 14 skipping mutant NSCLC and have shown activity against MET amplified NSCL

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13

Sato, Hiroki, Ryu Imamura, Hiroaki Suga, Kunio Matsumoto, and Katsuya Sakai. "Cyclic Peptide-Based Biologics Regulating HGF-MET." International Journal of Molecular Sciences 21, no. 21 (2020): 7977. http://dx.doi.org/10.3390/ijms21217977.

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Using a random non-standard peptide integrated discovery system, we obtained cyclic peptides that bind to hepatocyte growth factor (HGF) or mesenchymal-epithelial transition factor. (MET) HGF-inhibitory peptide-8 (HiP-8) selectively bound to two-chain active HGF, but not to single-chain precursor HGF. HGF showed a dynamic change in its molecular shape in atomic force microscopy, but HiP-8 inhibited dynamic change in the molecular shape into a static status. The inhibition of the molecular dynamics of HGF by HiP-8 was associated with the loss of the ability to bind MET. HiP-8 could selectively

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14

Kentsis, Alex, Takaomi Sanda, Vu Ngo, et al. "Aberrant Expression of Hepatocyte Growth Factor Induces Autocrine MET Activation Providing a Novel Therapeutic Target In Acute Myeloid Leukemia." Blood 116, no. 21 (2010): 1042. http://dx.doi.org/10.1182/blood.v116.21.1042.1042.

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Abstract Abstract 1042 Despite improvements in the treatment of acute myeloid leukemia (AML), high risk disease such as complex aberrant karyotype AML remains largely refractory to current therapy, and is mostly fatal. Identification of effective therapeutic targets by using candidate gene approaches has been limited by the number and variety of genetic defects associated with AML. Thus, we carried out a genome-wide functional screen in complex karyotype AML using a retroviral library of short hairpin RNAs (shRNAs), and discovered that shRNA-mediated depletion of hepatocyte growth factor (HGF)

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15

McInnis, Ian, Theresa Hahn, Anasitasia Ioane, et al. "Diverse Roles of Hepatocyte Growth Factor (HGF) in Normal Karyotype Acute Myeloid Leukemia (AML)." Blood 114, no. 22 (2009): 3107. http://dx.doi.org/10.1182/blood.v114.22.3107.3107.

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Abstract Abstract 3107 Poster Board III-44 Prior studies have demonstrated that hepatocyte growth factor (HGF) regulates proliferation and differentiation of normal hematopoietic progenitors. HGF activity occurs primarily via interactions with the c-met receptor, a tyrosine kinase receptor found on epithelial and some cancer cells. In solid tumors, HGF/c-met interactions mediate increased neoplastic invasion, metastases, and angiogenesis. However, in vitro, HGF has also been shown to mediate anti-tumor effects in leukemia cell line models. To better elucidate the role of HGF in acute leukemoge

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16

Zhou, Si-Rui, Wen-Ting Yuan, Xiao-Yan Pan, Tong Wang, and Xiao-Dong Chen. "Hepatocyte growth factor promotes retinal pigment epithelium cell activity through MET/AKT signaling pathway." International Journal of Ophthalmology 17, no. 5 (2024): 806–14. http://dx.doi.org/10.18240/ijo.2024.05.03.

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AIM: To explore the effects of hepatocyte growth factor (HGF) on retinal pigment epithelium (RPE) cell behaviors. METHODS: The human adult retinal pigment epithelial cell line-19 (ARPE-19) were treated by HGF or mesenchymal-epithelial transition factor (MET) inhibitor SU11274 in vitro. Cell viability was detected by a Cell Counting Kit-8 assay. Cell proliferation and motility was detected by a bromodeoxyuridine incorporation assay and a wound healing assay, respectively. The expression levels of MET, phosphorylated MET, protein kinase B (AKT), and phosphorylated AKT proteins were determined by

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17

Borset, M., H. Hjorth-Hansen, C. Seidel, A. Sundan, and A. Waage. "Hepatocyte growth factor and its receptor c-met in multiple myeloma." Blood 88, no. 10 (1996): 3998–4004. http://dx.doi.org/10.1182/blood.v88.10.3998.bloodjournal88103998.

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We have examined whether the hepatocyte growth factor (HGF)/c-met receptor-ligand pair is expressed in freshly isolated and highly purified myeloma cells and whether HGF can be found in the sera of myeloma patients. Myeloma cells were purified with an immunomagnetic method using the syndecan 1-specific antibody B-B4. HGF and c-met mRNA in these cells were examined by reverse transcriptase-polymerase chain reaction (RT-PCR). HGF and c-met proteins were detected by enzyme- linked immunosorbent assay (ELISA) and Western blot, respectively. Serum from 13 myeloma patients was obtained at diagnosis

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18

Anastasi, Sergio, Silvia Giordano, Olga Sthandier, et al. "A Natural Hepatocyte Growth Factor/Scatter Factor Autocrine Loop in Myoblast Cells and the Effect of the Constitutive Met Kinase Activation on Myogenic Differentiation." Journal of Cell Biology 137, no. 5 (1997): 1057–68. http://dx.doi.org/10.1083/jcb.137.5.1057.

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As a rule, hepatocyte growth factor/scatter factor (HGF/SF) is produced by mesenchymal cells, while its receptor, the tyrosine kinase encoded by the met proto-oncogene, is expressed by the neighboring epithelial cells in a canonical paracrine fashion. In the present work we show that both HGF/SF and met are coexpressed by undifferentiated C2 mouse myoblasts. In growing cells, the autocrine loop is active as the receptor exhibits a constitutive phosphorylation on tyrosine that can be abrogated by exogenously added anti-HGF/SF neutralizing antibodies. The transcription of HGF/SF and met genes is

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19

Tahira, Yumiko, Katsuya Sakai, Hiroki Sato, Ryu Imamura, and Kunio Matsumoto. "Dimer Interface in Natural Variant NK1 Is Dispensable for HGF-Dependent Met Receptor Activation." International Journal of Molecular Sciences 22, no. 17 (2021): 9240. http://dx.doi.org/10.3390/ijms22179240.

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NK1, a splicing variant of hepatocyte growth factor (HGF), binds to and activates Met receptor by forming an NK1 dimer and 2:2 complex with Met. Although the structural mechanism underlying Met activation by HGF remains incompletely resolved, it has been proposed that the NK1 dimer structure participates in this activation. We investigated the NK1 dimer interface’s role in Met activation by HGF. Because N127, V140, and K144 are closely involved in the head-to-tail NK1 dimer formation, mutant NK1 proteins with replacement of these residues by alanine were prepared. In Met tyrosine phosphorylati

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20

Chang, Chih-Ching, Jia-Jhen Chiu, Shan-Ling Chen, et al. "Activation of HGF/c-Met signaling by ultrafine carbon particles and its contribution to alveolar type II cell proliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 302, no. 8 (2012): L755—L763. http://dx.doi.org/10.1152/ajplung.00350.2011.

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Hepatocyte growth factor (HGF) is a potent mitogen and motogen for various epithelial cells. The present study aimed to explore the role of HGF and c-Met receptor in ultrafine carbon particle-induced alveolar type II epithelial (type II) cell proliferation. ICR mice were intratracheally instilled with 100 μg ultrafine carbon black (ufCB) and killed at 21, 48, and 72 days postexposure to examine type II cell proliferation, HGF release, and c-Met activation. In vivo and in vitro applications of neutralizing anti-HGF antibody were used to investigate the causal role of HGF in cell proliferation.

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21

Bieś, Rafał, Agnieszka Mikosińska, Jakub Parys, et al. "The influence of hepatocyte growth factor on the proliferation and differentiation of stem cells." Journal of Education, Health and Sport 77 (January 8, 2025): 57418. https://doi.org/10.12775/jehs.2025.77.57418.

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Background: The HGF/c-Met signaling pathway is central to various biological processes, including tissue regeneration, cell proliferation, and differentiation. Dysregulation of this pathway has been implicated in cancer progression and poor prognosis. Despite its potential as a therapeutic target, the complexity of HGF/c-Met signaling and the associated challenges, such as off-target effects and limited understanding of its role in different disease contexts, pose significant obstacles to clinical translation. Objectives: This review aims to examine the role of the HGF/c-Met pathway in tissue

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22

Dedov, I. I., Ye A. Troshina, N. V. Mazurina, and A. Belfiore. "Low expression of Met-hepatocytic growth factor receptor as an indicator of poor prognosis in thyroid tumors." Problems of Endocrinology 47, no. 3 (2001): 6–10. http://dx.doi.org/10.14341/probl11467.

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Clinical implication of Met-hepatocytic growth factor receptor (Met/HGF-R) in thyroid adenocarcinoma tissue was studied on 163 operative thyroid samples (129papillary cancers, 21 follicular cancers, and 13 anaplastic cancers). 49 adenomas, 50 nodular goiters and 50 normal thyroids were compared. Expression of Met/HGF-R was estimated using semiquantitative immunohistochemical method including proportion (limits 0-5) and intensity (limits 0-5) of cell staining and calculation of Met/HGF-R total expression (limit 0-10). Met/HGF-R was not found in normal thyroid tissue, was absent or focally expre

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23

You, Jingjing, Li Wen, Athena Roufas, Chris Hodge, Gerard Sutton, and Michele C. Madigan. "Expression of HGF and c-Met Proteins in Human Keratoconus Corneas." Journal of Ophthalmology 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/852986.

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Keratoconus (KC) is a progressive degenerative inflammatory-related disease of the human cornea leading to decreased visual function. The pathogenesis of KC remains to be understood. Recent genetic studies indicate that gene variants of an inflammation-related molecule, hepatocyte growth factor (HGF), are associated with an increased susceptibility for developing KC. However HGF protein expression in KC has not been explored. In this initial study, we investigated late-stage KC and control corneas for the expression of HGF and its receptor mesenchymal-epithelial transition factor (c-Met/Met).

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24

Blanquaert, Frederic, Renata C. Pereira, and Ernesto Canalis. "Cortisol inhibits hepatocyte growth factor/scatter factor expression and induces c-met transcripts in osteoblasts." American Journal of Physiology-Endocrinology and Metabolism 278, no. 3 (2000): E509—E515. http://dx.doi.org/10.1152/ajpendo.2000.278.3.e509.

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Hepatocyte growth factor/scatter factor (HGF/SF) is expressed by osteoblasts and has important effects on repair and bone remodeling. Because glucocorticoids regulate these two functions, we tested the effects of cortisol on the expression of HGF/SF and c-met, the protooncogene encoding the HGF/SF receptor, in cultures of osteoblast-enriched cells from 22-day fetal rat calvariae (Ob cells). Cortisol decreased HGF/SF mRNA levels and diminished the induction of HGF/SF transcripts by fibroblast growth factor-2 (FGF-2) and platelet-derived growth factor BB (PDGF BB). Cortisol also decreased FGF-2

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25

Boschert, Verena, Nicola Klenk, Alexander Abt, et al. "The Influence of Met Receptor Level on HGF-Induced Glycolytic Reprogramming in Head and Neck Squamous Cell Carcinoma." International Journal of Molecular Sciences 21, no. 2 (2020): 471. http://dx.doi.org/10.3390/ijms21020471.

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Head and neck squamous cell carcinoma (HNSCC) is known to overexpress a variety of receptor tyrosine kinases, such as the HGF receptor Met. Like other malignancies, HNSCC involves a mutual interaction between the tumor cells and surrounding tissues and cells. We hypothesized that activation of HGF/Met signaling in HNSCC influences glucose metabolism and therefore substantially changes the tumor microenvironment. To determine the effect of HGF, we submitted three established HNSCC cell lines to mRNA sequencing. Dynamic changes in glucose metabolism were measured in real time by an extracellular

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26

Cao, Tong, Jing Pan, Xiulian Li, et al. "Isolation and Characterization of a Chinese Hamster Ovary Heparan Sulfate Cell Mutant Defective in Both Met Receptor Binding and Hepatocyte Growth Factor NK1/Met Signaling." Cellular Physiology and Biochemistry 48, no. 4 (2018): 1480–91. http://dx.doi.org/10.1159/000492258.

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Background/Aims: The up-regulation of hepatocyte growth factor/receptor, HGF/Met, signal transduction is observed in most of human cancers. Specific heparan sulfate structures enhance the HGF/Met signaling at both cell and animal-based model systems. Biochemical studies indicate that heparan sulfate interacts with HGF and a natural occurring splicing variant NK1 of HGF with similar affinity. However, it is currently unknown if cell surface heparan sulfate binds to Met at physiological conditions and if specific cell surface heparan sulfate structures are required for effective HGF/Met or NK1/M

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27

Beilmann, Mario, George F. Vande Woude, Hans-Peter Dienes, and Peter Schirmacher. "Hepatocyte growth factor–stimulated invasiveness of monocytes." Blood 95, no. 12 (2000): 3964–69. http://dx.doi.org/10.1182/blood.v95.12.3964.

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Abstract Hepatocyte growth factor (HGF) is a pluripotent cytokine with mitogenic, motogenic, and morphogenic activity for mainly epithelial and endothelial target cells. We previously demonstrated that the specific HGF receptor, MET, is induced in stimulated peripheral blood monocytes. In this study, we analyzed the functional consequences of MET activation in primary cultures of peripheral blood monocytes from healthy donors. After stimulation of MET-expressing monocytes with recombinant HGF, the gene-expression profile of peripheral blood mononuclear cells and monocytes was significantly mod

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28

Beilmann, Mario, George F. Vande Woude, Hans-Peter Dienes, and Peter Schirmacher. "Hepatocyte growth factor–stimulated invasiveness of monocytes." Blood 95, no. 12 (2000): 3964–69. http://dx.doi.org/10.1182/blood.v95.12.3964.012k20_3964_3969.

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Анотація:

Hepatocyte growth factor (HGF) is a pluripotent cytokine with mitogenic, motogenic, and morphogenic activity for mainly epithelial and endothelial target cells. We previously demonstrated that the specific HGF receptor, MET, is induced in stimulated peripheral blood monocytes. In this study, we analyzed the functional consequences of MET activation in primary cultures of peripheral blood monocytes from healthy donors. After stimulation of MET-expressing monocytes with recombinant HGF, the gene-expression profile of peripheral blood mononuclear cells and monocytes was significantly modulated, e

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29

Hay, Rick V., Brian Cao, R. Scot Skinner, et al. "Radioimmunoscintigraphy of Tumors Autocrine for Human Met and Hepatocyte Growth Factor/Scatter Factor." Molecular Imaging 1, no. 1 (2002): 153535002002000. http://dx.doi.org/10.1162/15353500200200006.

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Inappropriate expression of the c-met-protooncogene product (Met) and/or of its ligand, hepatocyte growth factor/scatter factor (HGF/SF), has been correlated with poor prognosis in a variety of human solid tumors. We are developing animal models for nuclear imaging of Met and HGF/SF expression in tumors in vivo. We radioiodinated a mixture of monoclonal antibodies (MAbs) that bind to human HGF/SF and to the external ligand-binding domain of human Met, and then injected the I-125-MAb mixture intravenously into mice bearing tumors either autocrine for human HGF/SF and human Met or autocrine-para

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30

Tonomura, Hitoshi, Masateru Nagae, Ryota Takatori, Hidenobu Ishibashi, Tomonori Itsuji, and Kenji Takahashi. "The Potential Role of Hepatocyte Growth Factor in Degenerative Disorders of the Synovial Joint and Spine." International Journal of Molecular Sciences 21, no. 22 (2020): 8717. http://dx.doi.org/10.3390/ijms21228717.

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This paper aims to provide a comprehensive review of the changing role of hepatocyte growth factor (HGF) signaling in the healthy and diseased synovial joint and spine. HGF is a multifunctional growth factor that, like its specific receptor c-Met, is widely expressed in several bone and joint tissues. HGF has profound effects on cell survival and proliferation, matrix metabolism, inflammatory response, and neurotrophic action. HGF plays an important role in normal bone and cartilage turnover. Changes in HGF/c-Met have also been linked to pathophysiological changes in degenerative joint disease

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Xu, Chuanhui, Anke Van Den Berg, Wouter Plattel, et al. "Expression of the c-Met Oncogene Correlates with Favorable Progression Free Survival In Classical Hodgkin Lymphoma." Blood 116, no. 21 (2010): 3880. http://dx.doi.org/10.1182/blood.v116.21.3880.3880.

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Abstract Abstract 3880 Background The HGF/c-Met signaling pathway regulates a variety of biological processes, including proliferation, survival and migration. Aberrant c-Met activation has been implicated in the pathogenesis of many human cancers. Furthermore, c-Met is of prognostic significance in several types of cancer such as diffuse large B cell lymphoma, bladder cancer, breast cancer, colorectal cancer and ovarian cancer. Expression of c-Met in Hodgkin lymphoma (HL) patients, as well as increased levels of HGF in the urine of HL patients has been reported, but no prognostic studies or f

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Sweis, Randy F., Petros Grivas, Alexander T. Pearson, Kathleen C. Day, Mark L. Day, and Maha Hussain. "Expression of MET and HGF in bladder cancer tumorigenesis and invasion." Journal of Clinical Oncology 30, no. 15_suppl (2012): 4573. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.4573.

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4573 Background: The human MET gene encodes the hepatocyte growth factor (HGF) tyrosine kinase receptor. Limited studies in human bladder cancer have demonstrated that expression of MET protein is linked with disease progression and survival. We hypothesized that the expression of both MET and its ligand HGF are altered in bladder cancer. Methods: Expression of MET and HGF in human bladder tissues was explored using Oncomine, an online compendium of cancer transcriptome profiles. The largest relevant dataset was identified and contained 157 samples (Sanchez-Carbayo, et al. 2006). Normalized an

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Sierra, J. Rafael, and Ming-Sound Tsao. "c-MET as a potential therapeutic target and biomarker in cancer." Therapeutic Advances in Medical Oncology 3, no. 1_suppl (2011): S21—S35. http://dx.doi.org/10.1177/1758834011422557.

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The receptor tyrosine kinase c-MET and its ligand, hepatocyte growth factor (HGF), regulate multiple cellular processes that stimulate cell proliferation, invasion and angiogenesis. This review provides an overview of the evidence to support c-MET or the HGF/c-MET signaling pathway as relevant targets for personalized cancer treatment based on high frequencies of c-MET and/or HGF overexpression, activation, amplification in non-small cell lung carcinoma (NSCLC), gastric, ovarian, pancreatic, thyroid, breast, head and neck, colon and kidney carcinomas. Additionally, the current knowledge of sma

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Beilmann, Mario, Margarete Odenthal, Waltraud Jung, George F. Vande Woude, Hans-Peter Dienes, and Peter Schirmacher. "Neoexpression of the c-met/Hepatocyte Growth Factor-Scatter Factor Receptor Gene in Activated Monocytes." Blood 90, no. 11 (1997): 4450–58. http://dx.doi.org/10.1182/blood.v90.11.4450.

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Abstract Hepatocyte growth factor-scatter factor (HGF-SF ) mediates mito-, moto-, and morphogenic effects through the MET receptor, a membrane bound tyrosine kinase. HGF-SF/MET signaling is mitogenic for a large number of epithelial and endothelial cells and activates organ regeneration. HGF-SF transcripts have been detected in various myeloid cell lines. Therefore, the potential role of HGF-SF/MET signaling for circulating cells of the immune system, especially under conditions of inflammation, was evaluated. Several B-lymphoid and myeloid cell lines were found to express HGF-SF or c-met tran

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Beilmann, Mario, Margarete Odenthal, Waltraud Jung, George F. Vande Woude, Hans-Peter Dienes, and Peter Schirmacher. "Neoexpression of the c-met/Hepatocyte Growth Factor-Scatter Factor Receptor Gene in Activated Monocytes." Blood 90, no. 11 (1997): 4450–58. http://dx.doi.org/10.1182/blood.v90.11.4450.4450_4450_4458.

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Анотація:

Hepatocyte growth factor-scatter factor (HGF-SF ) mediates mito-, moto-, and morphogenic effects through the MET receptor, a membrane bound tyrosine kinase. HGF-SF/MET signaling is mitogenic for a large number of epithelial and endothelial cells and activates organ regeneration. HGF-SF transcripts have been detected in various myeloid cell lines. Therefore, the potential role of HGF-SF/MET signaling for circulating cells of the immune system, especially under conditions of inflammation, was evaluated. Several B-lymphoid and myeloid cell lines were found to express HGF-SF or c-met transcripts,

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Tjin, Esther P. M., Richard W. J. Groen, Irma Vogelzang, et al. "Functional analysis of HGF/MET signaling and aberrant HGF-activator expression in diffuse large B-cell lymphoma." Blood 107, no. 2 (2006): 760–68. http://dx.doi.org/10.1182/blood-2005-05-1929.

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AbstractInappropriate activation of MET, the receptor tyrosine kinase for hepatocyte growth factor (HGF), has been implicated in tumorigenesis. Although we have previously shown that HGF/MET signaling controls survival and proliferation of multiple myeloma (MM), its role in the pathogenesis of other B-cell malignancies has remained largely unexplored. Here, we have examined a panel of 110 B-cell malignancies for MET expression, which, apart from MM (48%), was found to be largely confined to diffuse large B-cell lymphomas (DLBCLs) (30%). No amplification of the MET gene was found; however, muta

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Borset, Magne, Hakon Hov, Randi U. Holt, et al. "A Selective Inhibitor of c-Met Blocks an Autocrine HGF Growth Loop in ANBL-6 Cells and Prevents Migration and Adhesion of Myeloma Cells." Blood 104, no. 11 (2004): 2358. http://dx.doi.org/10.1182/blood.v104.11.2358.2358.

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Abstract We examined the role of the hepatocyte growth factor (HGF) receptor c-Met in multiple myeloma by applying a novel selective small-molecule tyrosine kinase inhibitor, PHA-665752, directed against the receptor. Four biological sequels of HGF related to multiple myeloma were studied: (1) proliferation of myeloma cells; (2) secretion of interleukin-11 from osteogenic cells; (3) migration of myeloma cells; and (4) adhesion of myeloma cells to fibronectin. We also examined effects of the c-Met inhibitor on intracellular signaling pathways in myeloma cells. PHA-665752 effectively blocked the

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Uzumcu, Mehmet, Zui Pan, Yi Chu, Peter E. Kuhn, and Rob Zachow. "Immunolocalization of the hepatocyte growth factor (HGF) system in the rat ovary and the anti-apoptotic effect of HGF in rat ovarian granulosa cells in vitro." Reproduction 132, no. 2 (2006): 291–99. http://dx.doi.org/10.1530/rep.1.00989.

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Hepatocyte growth factor (HGF) regulates granulosa cell (GC) steroidogenesis and suppresses apoptosis in non-ovarian cells. The hypothesis was thus developed that intraovarian HGF supports folliculogenesis by mediating steroidogenesis and suppressing apoptosis. To investigate the latter, the anti-apoptotic actions of HGF were tested in GCs and follicles isolated from immature rats. Results showed that HGF suppressed apoptosis in GC and follicle cultures as visualized using apoptosis indicator dye, YO-PRO-1. Immunohistochemistry was used to investigate the distribution of HGF, c-met, and HGF ac

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Cerqua, Marina, Orsola Botti, Maddalena Arigoni, et al. "MET∆14 promotes a ligand-dependent, AKT-driven invasive growth." Life Science Alliance 5, no. 10 (2022): e202201409. http://dx.doi.org/10.26508/lsa.202201409.

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MET is an oncogene encoding the tyrosine kinase receptor for hepatocyte growth factor (HGF). Upon ligand binding, MET activates multiple signal transducers, including PI3K/AKT, STAT3, and MAPK. When mutated or amplified, MET becomes a “driver” for the onset and progression of cancer. The most frequent mutations in the MET gene affect the splicing sites of exon 14, leading to the deletion of the receptor’s juxtamembrane domain (MET∆14). It is currently believed that, as in gene amplification, MET∆14 kinase is constitutively active. Our analysis of MET in carcinoma cell lines showed that MET∆14

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40

Miranda, Oshin, Mariya Farooqui, and Jill Siegfried. "Status of Agents Targeting the HGF/c-Met Axis in Lung Cancer." Cancers 10, no. 9 (2018): 280. http://dx.doi.org/10.3390/cancers10090280.

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Hepatocyte growth factor (HGF) is the ligand for the tyrosine kinase receptor c-Met (Mesenchymal Epithelial Transition Factor also known as Hepatocyte Growth Factor Receptor, HGFR), a receptor with expression throughout epithelial and endothelial cell types. Activation of c-Met enhances cell proliferation, invasion, survival, angiogenesis, and motility. The c-Met pathway also stimulates tissue repair in normal cells. A body of past research shows that increased levels of HGF and/or overexpression of c-Met are associated with poor prognosis in several solid tumors, including lung cancer, as wel

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Ricci, G., A. Catizone, and M. Galdieri. "Expression and functional role of hepatocyte growth factor and its receptor (c-met) during fetal mouse testis development." Journal of Endocrinology 191, no. 3 (2006): 559–70. http://dx.doi.org/10.1677/joe.1.06879.

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The hepatocyte growth factor (HGF) is a pleiotropic cytokine able to regulate different cellular functions. HGF action is mediated by its receptor, c-met, a glycoprotein with tyrosine kinase activity. We previously demonstrated that c-met is expressed in the newly formed seminiferous cords of the mice embryonic testes and that HGF acts as a morphogenetic factor. In this paper, we report that at 15.5 days post-coitum (dpc) c-met is expressed in the testicular cords, whereas at 18.5 dpc c-met expression is almost exclusively localized in the interstitial tissue of the testis in particular in the

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Buchynska, L. G., O. V. Brieieva, and S. V. Nespriadko. "EXPRESSION OF HEPATOCYTE GROWTH FACTOR AND C-MET RECEPTOR IN STROMAL FIBROBLASTS AND TUMOR CELLS OF ENDOMETRIAL CARCINOMA." Experimental Oncology 45, no. 1 (2023): 79–87. http://dx.doi.org/10.15407/exp-oncology.2023.01.079.

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Background: HGF/c-Met is one of the main signaling pathways that ensure communication between epithelial cells and components of the tumor microenvironment determining the invasive and metastatic potential of many cancers. However, the significance of HGF and c-Met in endometrial carcinoma (ECa) progression remains unclear. Aim: To evaluate copy number variations as well as expression of the c-Met receptor and its ligand HGF in endometrial carcinomas considering the clinical and morphological characteristics of ECa. Materials and Methods: The study was conducted on ECa samples of 57 patients,

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Xu, Chuanhui, Anke Van Den Berg, Arjan Diepstra, et al. "The HGF/c-Met Signaling Pathway in Hodgkin Lymphoma." Blood 114, no. 22 (2009): 1551. http://dx.doi.org/10.1182/blood.v114.22.1551.1551.

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Abstract Abstract 1551 Poster Board I-574 Introduction Hodgkin lymphoma (HL) is a B-cell neoplasm characterized by a minority of neoplastic cells, the so-called Hodgkin and Reed-Sternberg (HRS) cells, which are located within an extensive infiltrate of reactive cells. Aberrant signaling of various receptor tyrosine kinases (RTKs) via autocrine or paracrine mechanisms contributes to the survival and proliferation of HRS cells. Activation of the hepatocyte growth factor (HGF)/c-Met signaling pathway has been implicated in the pathophysiology of many cancers, but its role in HL is poorly investig

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Chattopadhyay, Naibedya, R. J. MacLeod, Jacob Tfelt-Hansen та Edward M. Brown. "1α,25(OH)2-vitamin D3inhibits HGF synthesis and secretion from MG-63 human osteosarcoma cells". American Journal of Physiology-Endocrinology and Metabolism 284, № 1 (2003): E219—E227. http://dx.doi.org/10.1152/ajpendo.00247.2002.

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Several mesenchymally derived cells, including osteoblasts, secrete hepatocyte growth factor (HGF). 1α,25(OH)2-vitamin D3[1,25(OH)2D3] inhibits proliferation and induces differentiation of MG-63 osteoblastic cells. Here we show that MG-63 cells secrete copious amounts of HGF and that 1,25(OH)2D3inhibits HGF production. MG-63 cells also express HGF receptor (c-Met) mRNA, suggesting an autocrine action of HGF. Indeed, although exogenous HGF failed to stimulate cellular proliferation, neutralizing endogenous HGF with a neutralizing antibody inhibited MG-63 cell proliferation; moreover, inhibiting

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Elliott, Bruce E., Wesley L. Hung, Alexander H. Boag, and Alan B. Tuck. "The role of hepatocyte growth factor (scatter factor) in epithelialmesenchymal transition and breast cancer." Canadian Journal of Physiology and Pharmacology 80, no. 2 (2002): 91–102. http://dx.doi.org/10.1139/y02-010.

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North American women have a one in eight lifetime risk of developing breast cancer, and approximately one in three women with breast cancer will die of metastases. We, and others, have recently shown that high levels of expression of hepatocyte growth factor (HGF) and its receptor Met are associated with invasive human breast cancer and may be causally linked to metastasis. This high level of HGF and Met expression has been considered as a possible indicator of earlier recurrence and shortened survival in breast cancer patients. In contrast, HGF expression (but not Met) is strongly suppressed

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Tsubaki, Masanobu, Shiori Seki, Tomoya Takeda та ін. "The HGF/Met/NF-κB Pathway Regulates RANKL Expression in Osteoblasts and Bone Marrow Stromal Cells". International Journal of Molecular Sciences 21, № 21 (2020): 7905. http://dx.doi.org/10.3390/ijms21217905.

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Multiple myeloma (MM)-induced bone disease occurs through hyperactivation of osteoclasts by several factors secreted by MM cells. MM cell-secreted factors induce osteoclast differentiation and activation via direct and indirect actions including enhanced expression of receptor activator of nuclear factor κB ligand (RANKL) in osteoblasts and bone marrow stromal cells (BMSCs). Hepatocyte growth factor (HGF) is elevated in MM patients and is associated with MM-induced bone disease, although the mechanism by which HGF promotes bone disease remains unclear. In the present study, we demonstrated tha

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Jalili, Ali, Neeta Shirvaikar, Sara Ilnitsky, A. Robert Turner, Mariusz Z. Ratajczak, and Anna Janowska-Wieczorek. "G-CSF Induces Expression of Both Hepatocyte Growth Factor (HGF) and Its Receptor (c-Met) in Human Hematopoietic Stem/Progenitor Cells and Mature Myeloid Cells - Novel Evidence That during Mobilization the HGF-c-Met Axis Counterbalances G-CSF-Induced Attenuation of the SDF-1-CXCR4 Axis." Blood 110, no. 11 (2007): 2203. http://dx.doi.org/10.1182/blood.v110.11.2203.2203.

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Abstract The stromal-derived factor-1 (SDF-1)-CXCR4 axis plays an important role in stem cell trafficking, and G-CSF- induced mobilization decreases SDF-1 expression in the bone marrow (BM) microenvironment and CXCR4 expression by CD34+ hematopoietic stem/progenitor cells (HSPC). Alternatively, the tyrosine kinase c-Met receptor-HGF axis was recently postulated to play an important role in the trafficking of non-hematopoietic cells; however, our previous research demonstrated that while HGF is an important constituent of the BM microenvironment, c-Met is not expressed by BM-derived steady stat

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Zachow, Rob, and Mehmet Uzumcu. "The hepatocyte growth factor system as a regulator of female and male gonadal function." Journal of Endocrinology 195, no. 3 (2007): 359–71. http://dx.doi.org/10.1677/joe-07-0466.

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The hepatocyte growth factor (HGF) system comprises HGF, its receptor (the c-met tyrosine kinase), HGF activator (HGFA) protein, and HGFA inhibitor (HAI). The components of the HGF system have been identified in a plethora of tissues to include the ovary and testis. In its traditional context, the HGF system works via paracrine- and autocrine-mediated feedback in which HGF (of mesenchymal origin) binds and activates c-met (within epithelial cells); target cells then respond to HGF via any number of morphogenic and functional changes. The concomitant presence of HGFA and HAI suggests that HGF b

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Liu, Y., E. M. Tolbert, A. M. Sun, and L. D. Dworkin. "Primary structure of rat HGF receptor and induced expression in glomerular mesangial cells." American Journal of Physiology-Renal Physiology 271, no. 3 (1996): F679—F688. http://dx.doi.org/10.1152/ajprenal.1996.271.3.f679.

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The c-met protooncogene encodes a transmembrane tyrosine kinase receptor for hepatocyte growth factor (HGF). It has been widely suggested that HGF and its receptor constitute a paracrine signaling system, in which mesenchymally derived cells produce ligand that binds to the receptor predominantly expressed on cells of epithelial origin. In this study, we have isolated and completely sequenced the entire coding region of c-met cDNA from the rat kidney. The nucleotide sequence of the rat c-met cDNA revealed that the HGF receptor is encoded within single open-reading frame as 190 kDa of a transme

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Jeffers, M., S. Rong, and G. F. Vande Woude. "Enhanced tumorigenicity and invasion-metastasis by hepatocyte growth factor/scatter factor-met signalling in human cells concomitant with induction of the urokinase proteolysis network." Molecular and Cellular Biology 16, no. 3 (1996): 1115–25. http://dx.doi.org/10.1128/mcb.16.3.1115.

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Hepatocyte growth factor/scatter factor (HGF/SF) is a pleiotropic effector of cells expressing the Met tyrosine kinase receptor. Although HGF/SF is synthesized by mesenchymal cells and acts predominantly on epithelial cells, we have recently demonstrated that human sarcoma cell lines often inappropriately express high levels of Met and respond mitogenically to HGF/SF. In the present report we show that HGF/SF-Met signalling in the human leiomyosarcoma cell line SK-LMS-1 enhances its in vivo tumorigenicity, an effect for which the mitogenicity of this signalling pathway is likely to play a role

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