Log in

Relevant bibliographies by topics / C-Met Kinase / Journal articles

To see the other types of publications on this topic, follow the link: C-Met Kinase.

Journal articles on the topic 'C-Met Kinase'

Author: Grafiati

Published: 7 June 2025

Last updated: 16 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'C-Met Kinase.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Smotrov, Nadya, Anjili Mathur, Ilona Kariv, Christopher M. Moxham, and Nathan Bays. "Development of a Cell-Based Assay for Measurement of c-Met Phosphorylation Using AlphaScreenTM Technology and High-Content Imaging Analysis." Journal of Biomolecular Screening 14, no. 4 (2009): 404–11. http://dx.doi.org/10.1177/1087057109331803.

Full text

Abstract:

c-Met is a receptor tyrosine kinase (RTK) with a critical role in many fundamental cellular processes, including cell proliferation and differentiation. Deregulated c-Met signaling has been implicated in both the initiation and progression of human cancers and therefore represents an attractive target for anticancer therapy. Monitoring the phosphorylation status of relevant tyrosine residues provides an important method of assessing c-Met kinase activity. This report describes a novel assay to monitor c-Met phosphorylation in cells using Amplified Luminescent Proximity Homogeneous Assay (Alpha

APA, Harvard, Vancouver, ISO, and other styles

2

Xu, Xiangming, and Lei Yao. "Recent Patents on the Development of c-Met Kinase Inhibitors." Recent Patents on Anti-Cancer Drug Discovery 15, no. 3 (2020): 228–38. http://dx.doi.org/10.2174/1574892815666200630102344.

Full text

Abstract:

Background : Receptor Tyrosine Kinases (RTKs) play critical roles in a variety of cellular processes including growth, differentiation and angiogenesis, and in the development and progression of many types of cancer. Mesenchymal-Epithelial Transition Factor (c-Met) kinase is one of the types of RTKs and has become an attractive target for anti-tumor drug designing. c-Met inhibitors have a broad prospect in tumor prevention, chemotherapy, biotherapy, and especially in tumor resistance. Objective: The purpose of this article is to review recent research progress of c-Met inhibitors reported in p

APA, Harvard, Vancouver, ISO, and other styles

3

Chen, Zhengxia, Meibi Dai, Deheng Sun, et al. "Preclinical evaluation of WXSH0011, a selective small molecule dual inhibitor of FGFR/c-Met." Journal of Clinical Oncology 38, no. 15_suppl (2020): e15641-e15641. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e15641.

Full text

Abstract:

e15641 Background: FGFRs (fibroblast growth factor receptors) are a family of receptor tyrosine kinases. c-Met is a receptor tyrosine kinase with a high-affinity ligand, hepatocyte growth factor/scatter factor (HGF/SF). Aberrations in the FGFR pathway are associated with a variety of human cancers. c-Met and HGF have been implicated in carcinogenesis and metastatic tumor progression because of their ability to enhance angiogenesis, cancer cell proliferation, migration, and invasion. WXSH0011 is an orally bioavailable novel potent and selective FGFR/c-Met dual kinase inhibitor, which displayed

APA, Harvard, Vancouver, ISO, and other styles

4

al., G. "Synthesis of a c-Met Kinase Inhibitor." Synfacts 2010, no. 10 (2010): 1108. http://dx.doi.org/10.1055/s-0030-1258070.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Otuokere, IE, KK Igwe, JF Amaku, and OV Ikpeazu. "Pharmacophore modelling of 2-chlorobenzimidazole and its specific docking to the active site c-Met Kinase: A search for potent c-Met Kinase inhibitor." Pharmaceutical and Chemical Journal 7, no. 4 (2020): 86–96. https://doi.org/10.5281/zenodo.13955732.

Full text

Abstract:

In this paper, we demonstrate how pharmacophore modelling was used to design the analogues of 2-chlorobenzimidazole and the application of molecular docking studies in the evaluation of the ligand affinity for the target.  The lead molecule (1-benzyl-2-chloro-1<em>H</em>-benzimidazole) had the highest docking score of -8.0 kcal/mol and was observed to interact with 17 amino acids within the pocket of c-Met Kinase (ALA159, VAL39, TYR32, MET144, ASN142, ARG141, ALA154, ASP155, ALA49, LYS51, LEU90, TYR92, MET93, GLY32, ILE, ASP97 and GLY96).  Meanwhile, the ADME characteristics of 1-ben

APA, Harvard, Vancouver, ISO, and other styles

6

Ma, P. C., S. Jiang, R. Du, S. Dietrich, Z. Tang, and J. A. Kern. "Modeling targeted inhibition of wild type and mutated c-MET receptor." Journal of Clinical Oncology 25, no. 18_suppl (2007): 14010. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.14010.

Full text

Abstract:

14010 Background: c-MET belongs to the semaphorin superfamily of signaling proteins, containing three protein families (semaphorins, plexins, c-MET and RON) that have central roles in cell signaling. The c-MET receptor tyrosine kinase is involved in regulating cell growth/proliferation, survival, angiogenesis, cell scattering, cell motility and migration. Mutations in c-MET have been identified in various human cancers including lung cancer and papillary renal cell carcinomas. c-MET mutations occur within the extracellular seven-blade β-propeller fold sema domain (E168D, L229F, S325G, N375S),

APA, Harvard, Vancouver, ISO, and other styles

7

Sachs, M., K. M. Weidner, V. Brinkmann, et al. "Motogenic and morphogenic activity of epithelial receptor tyrosine kinases." Journal of Cell Biology 133, no. 5 (1996): 1095–107. http://dx.doi.org/10.1083/jcb.133.5.1095.

Full text

Abstract:

Receptor tyrosine kinases play essential roles in morphogenesis and differentiation of epithelia. Here we examined various tyrosine kinase receptors, which are preferentially expressed in epithelia (c-met, c-ros, c-neu, and the keratin growth factor [KGF] receptor), for their capacity to induce cell motility and branching morphogenesis of epithelial cells. We exchanged the ligand-binding domain of these receptors by the ectodomain of trkA and could thus control signaling by the new ligand, NGF. We demonstrate here that the tyrosine kinases of c-met, c-ros, c-neu, the KGF receptor, and trkA, bu

APA, Harvard, Vancouver, ISO, and other styles

8

Bosse, Tanja, Julia Ehinger, Aleksandra Czuchra, et al. "Cdc42 and Phosphoinositide 3-Kinase Drive Rac-Mediated Actin Polymerization Downstream of c-Met in Distinct and Common Pathways." Molecular and Cellular Biology 27, no. 19 (2007): 6615–28. http://dx.doi.org/10.1128/mcb.00367-07.

Full text

Abstract:

ABSTRACT Activation of c-Met, the hepatocyte growth factor (HGF)/scatter factor receptor induces reorganization of the actin cytoskeleton, which drives epithelial cell scattering and motility and is exploited by pathogenic Listeria monocytogenes to invade nonepithelial cells. However, the precise contributions of distinct Rho-GTPases, the phosphatidylinositol 3-kinases, and actin assembly regulators to c-Met-mediated actin reorganization are still elusive. Here we report that HGF-induced membrane ruffling and Listeria invasion mediated by the bacterial c-Met ligand internalin B (InlB) were sig

APA, Harvard, Vancouver, ISO, and other styles

9

Ye, Qianwen, Chenggong Fu, and Jiazhong Li. "Studying the Binding Modes of Novel 2-Aminopyridine Derivatives as Effective and Selective c-Met Kinase Type 1 Inhibitors Using Molecular Modeling Approaches." Molecules 26, no. 1 (2020): 52. http://dx.doi.org/10.3390/molecules26010052.

Full text

Abstract:

The mesenchymal epithelial cell transforming factor c-Met, encoded by c-Met proto-oncogene and known as a high-affinity receptor for Hepatocyte Growth Factor (HGF), is one of the receptor tyrosine kinases (RTKs) members. The HGF/c-Met signaling pathway has close correlation with tumor growth, invasion and metastasis. Thus, c-Met kinase has emerged as a prominent therapeutic target for cancer drug discovery. Recently a series of novel 2-aminopyridine derivatives targeting c-Met kinase with high biological activity were reported. In this study, 3D quantitative structure-activity relationship (QS

APA, Harvard, Vancouver, ISO, and other styles

10

Tulasne, David, Réjane Paumelle, K. Michael Weidner, Bernard Vandenbunder, and Véronique Fafeur. "The Multisubstrate Docking Site of the MET Receptor Is Dispensable for MET-mediated RAS Signaling and Cell Scattering." Molecular Biology of the Cell 10, no. 3 (1999): 551–65. http://dx.doi.org/10.1091/mbc.10.3.551.

Full text

Abstract:

The scatter factor/hepatocyte growth factor regulates scattering and morphogenesis of epithelial cells through activation of the MET tyrosine kinase receptor. In particular, the noncatalytic C-terminal tail of MET contains two autophosphorylation tyrosine residues, which form a multisubstrate-binding site for several cytoplasmic effectors and are thought to be essential for signal transduction. We show here that a MET receptor mutated on the four C-terminal tyrosine residues, Y1311F, Y1347F, Y1354F, and Y1363F, can induce efficiently a transcriptional response and cell scattering, whereas it c

APA, Harvard, Vancouver, ISO, and other styles

11

Koltai, Zsófia, Bernadett Szabó, Judit Jakus, and Péter Vajdovich. "Tyrosine kinase expression analyses in canine mammary gland tumours – A pilot study." Acta Veterinaria Hungarica 66, no. 2 (2018): 294–308. http://dx.doi.org/10.1556/004.2018.027.

Full text

Abstract:

Messenger RNA levels of oncogenic tyrosine kinases were determined in canine mammary tumours using real-time RT-PCR. The following tyrosine kinases and vascular endothelial growth factors (VEGF) were examined in malignant and healthy mammary tissues of 13 dogs: VEGFR1, VEGFR2, EGFR, ErbB2, PDGFR1, c-KIT and c-MET. Expression levels of all these factors were significantly higher in tumour samples than in normal mammary tissues taken from the same animal. Higher grading was associated with higher VEGFR1 levels. Grade III tumours showed significantly higher VEGF, c-MET and c-KIT mRNA expression,

APA, Harvard, Vancouver, ISO, and other styles

12

Mohareb, Rafat M., Wagnat W. Wardakhan, and Nermeen S. Abbas. "Synthesis of Tetrahydrobenzo[b]thiophene-3-carbohydrazide Derivatives as Potential Anti-cancer Agents and Pim-1 Kinase Inhibitors." Anti-Cancer Agents in Medicinal Chemistry 19, no. 14 (2019): 1737–53. http://dx.doi.org/10.2174/1871520619666190402153429.

Full text

Abstract:

Background: Tetrahydrobenzo[b]thiophene derivatives are well known to be biologically active compounds and many of them occupy a wide range of anticancer agent drugs. Objective: One of the main aim of this work was to synthesize target molecules not only possessing anti-tumor activities but also kinase inhibitors. To achieve this goal, our strategy was to synthesize a series of 4,5,6,7- tetrahydrobenzo[b]thiophene-3-carbohydrazide derivatives using cyclohexan-1,4-dione and cyanoacetylhydrazine to give the 2-amino-6-oxo-4,5,6,7-tetrahydrobenzo[b]thiophene-3-carbohydrazide (3) as the key startin

APA, Harvard, Vancouver, ISO, and other styles

13

Lüttich, Lina, María José Besso, Stephan Heiden, et al. "Tyrosine Kinase c-MET as Therapeutic Target for Radiosensitization of Head and Neck Squamous Cell Carcinomas." Cancers 13, no. 8 (2021): 1865. http://dx.doi.org/10.3390/cancers13081865.

Full text

Abstract:

The receptor tyrosine kinase c-MET activates intracellular signaling and induces cell proliferation, epithelial-to-mesenchymal-transition and migration. Within the present study, we validated the prognostic value of c-MET in patients with head and neck squamous cell carcinoma (HNSCC) treated with radio(chemo)therapy using the Cancer Genome Atlas database and found an association of increased MET gene expression and protein phosphorylation with reduced disease-specific and progression-free survival. To investigate the role of c-MET-dependent radioresistance, c-MET-positive cells were purified f

APA, Harvard, Vancouver, ISO, and other styles

14

Sun, Zhi-Gang, Yong-An Yang, Zhi-Gang Zhang, and Hai-Liang Zhu. "Optimization techniques for novel c-Met kinase inhibitors." Expert Opinion on Drug Discovery 14, no. 1 (2018): 59–69. http://dx.doi.org/10.1080/17460441.2019.1551355.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Zhang, Limin, Shama Virani, Yu Zhang, et al. "Molecular imaging of c-Met tyrosine kinase activity." Analytical Biochemistry 412, no. 1 (2011): 1–8. http://dx.doi.org/10.1016/j.ab.2011.01.028.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Niemann, Catherin, Volker Brinkmann, Eva Spitzer, et al. "Reconstitution of Mammary Gland Development In Vitro: Requirement of c-met and c-erbB2 Signaling for Branching and Alveolar Morphogenesis." Journal of Cell Biology 143, no. 2 (1998): 533–45. http://dx.doi.org/10.1083/jcb.143.2.533.

Full text

Abstract:

We have established a cell culture system that reproduces morphogenic processes in the developing mammary gland. EpH4 mouse mammary epithelial cells cultured in matrigel form branched tubules in the presence of hepatocyte growth factor/scatter factor (HGF/SF), the ligand of the c-met tyrosine kinase receptor. In contrast, alveolar structures are formed in the presence of neuregulin, a ligand of c-erbB tyrosine kinase receptors. These distinct morphogenic responses can also be observed with selected human mammary carcinoma tissue in explant culture. HGF/SF-induced branching was abrogated by the

APA, Harvard, Vancouver, ISO, and other styles

17

Lefebvre, Cory, Sierra Pellizzari, Vasudeva Bhat, Kristina Jurcic, David W. Litchfield, and Alison L. Allan. "Involvement of the AKT Pathway in Resistance to Erlotinib and Cabozantinib in Triple-Negative Breast Cancer Cell Lines." Biomedicines 11, no. 9 (2023): 2406. http://dx.doi.org/10.3390/biomedicines11092406.

Full text

Abstract:

Resistance to protein tyrosine kinase inhibitors (TKIs) presents a significant challenge in therapeutic target development for cancers such as triple-negative breast cancer (TNBC), where conventional therapies are ineffective at combatting systemic disease. Due to increased expression, the receptor tyrosine kinases EGFR (epidermal growth factor receptor) and c-Met are potential targets for treatment. However, targeted anti-EGFR and anti-c-Met therapies have faced mixed results in clinical trials due to acquired resistance. We hypothesize that adaptive responses in regulatory kinase networks wi

APA, Harvard, Vancouver, ISO, and other styles

18

Jagadeeswaran, Ramasamy, Sujatha Jagadeeswaran, Vytas P. Bindokas, and Ravi Salgia. "Activation of HGF/c-Met pathway contributes to the reactive oxygen species generation and motility of small cell lung cancer cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 6 (2007): L1488—L1494. http://dx.doi.org/10.1152/ajplung.00147.2006.

Full text

Abstract:

Small cell lung cancer (SCLC) is a difficult disease to treat and sometimes has overexpression or mutation of c-Met receptor tyrosine kinase. The effects of c-Met/hepatocyte growth factor (c-Met/HGF, ligand for c-Met) on activation of reactive oxygen species (ROS) was determined. HGF stimulation of c-Met-overexpressing H69 SCLC cells (40 ng/ml, 15 min) resulted in an increase of ROS, measured with fluorescent probe 2′-7′-dichlorofluorescein diacetate (DCFH-DA) or dihydroethidine (DHE) but not in c-Met-null H446 cells. ROS was increased in juxtamembrane (JM)-mutated variants (R988C and T1010I)

APA, Harvard, Vancouver, ISO, and other styles

19

Queisser, Angela, Emmanuel Seront, Laurence M. Boon, and Miikka Vikkula. "Genetic Basis and Therapies for Vascular Anomalies." Circulation Research 129, no. 1 (2021): 155–73. http://dx.doi.org/10.1161/circresaha.121.318145.

Full text

Abstract:

Vascular and lymphatic malformations represent a challenge for clinicians. The identification of inherited and somatic mutations in important signaling pathways, including the PI3K (phosphoinositide 3-kinase)/AKT (protein kinase B)/mTOR (mammalian target of rapamycin), RAS (rat sarcoma)/RAF (rapidly accelerated fibrosarcoma)/MEK (mitogen-activated protein kinase kinase)/ERK (extracellular signal-regulated kinases), HGF (hepatocyte growth factor)/c-Met (hepatocyte growth factor receptor), and VEGF (vascular endothelial growth factor) A/VEGFR (vascular endothelial growth factor receptor) 2 casca

APA, Harvard, Vancouver, ISO, and other styles

20

Park, Yu-Kyoung, and Byeong-Churl Jang. "The Receptor Tyrosine Kinase c-Met Promotes Lipid Accumulation in 3T3-L1 Adipocytes." International Journal of Molecular Sciences 24, no. 9 (2023): 8086. http://dx.doi.org/10.3390/ijms24098086.

Full text

Abstract:

The receptor tyrosine kinase c-Met is elaborated in embryogenesis, morphogenesis, metabolism, cell growth, and differentiation. JNJ38877605 (JNJ) is an inhibitor of c-Met with anti-tumor activity. The c-Met expression and its role in adipocyte differentiation are unknown. Here, we investigated the c-Met expression and phosphorylation, knockdown (KD) effects, and pharmacological inhibition of c-Met by JNJ on fat accumulation in murine preadipocyte 3T3-L1 cells. During 3T3-L1 preadipocyte differentiation, strikingly, c-Met expression at the protein and mRNA levels and the protein phosphorylation

APA, Harvard, Vancouver, ISO, and other styles

21

Lv, Peng-Cheng, Yu-Shun Yang, and Zhong-Chang Wang. "Recent Progress in the Development of Small Molecule c-Met Inhibitors." Current Topics in Medicinal Chemistry 19, no. 15 (2019): 1276–88. http://dx.doi.org/10.2174/1568026619666190712205353.

Full text

Abstract:

C-Met, also referred to as Hepatocyte Growth Factor Receptor (HGFR), is a heterodimeric receptor tyrosine kinase. It has been determined that c-Met gene mutations, overexpression, and amplification also occur in a variety of human tumor types, and these events are closely related to the aberrant activation of the HGF/c-Met signaling pathway. Meanwhile, high c-Met expression is closely associated with poor prognosis in cancer patients. The c-Met kinase has emerged as an attractive target for developing antitumor agents. In this review, we cover the recent advances on the small molecule c-Met in

APA, Harvard, Vancouver, ISO, and other styles

22

Mahmoud, Mahmoud A. Abdelaziz, Rafat M. Mohareb, and Meshari A. Al-Sharif. "Heterocyclization of Thiophenes Derived from Estrone Followed by Cytotoxic, HTRF Kinase and Pim-1 Kinase Evaluations." Anti-Cancer Agents in Medicinal Chemistry 18, no. 12 (2019): 1711–28. http://dx.doi.org/10.2174/1871520618666180507141045.

Full text

Abstract:

Background: A wide range of heterocyclic steroidal derivatives gained a special attention due to their wide range of pharmacological activities especially the therapeutic activities. Many pharmacological drugs containing the steroid nucleus are known in the market. Objective: Our main aim of this work was to synthesise a series of heterocyclic compounds especially thiophene and thienopyridine derivatives containing the estrone nucleus. The synthesized compounds posses antitumor and kinases inhibitions. Method: Thiophene derivatives of estrone were synthesized and used for further heterocycliza

APA, Harvard, Vancouver, ISO, and other styles

23

Uddin, Shahab, Azhar Hussain, Prashant Bavi, and Khawla Al-Kuraya. "Inhibition of Fatty Acid Synthase Suppresses c-Met Receptor Kinase and Induces Apoptosis in Diffuse Large B Cell Lymphoma." Blood 114, no. 22 (2009): 4787. http://dx.doi.org/10.1182/blood.v114.22.4787.4787.

Full text

Abstract:

Abstract Abstract 4787 Targeted approaches are expected to revolutionize cancer treatment in near future. Fatty acid synthase (FASN), the enzyme responsible for de novo synthesis of fatty acids has emerged as a potential therapeutic target for several cancers however its role in diffuse large B-cell lymphoma (DLBCL) has not been fully elucidated.. Therefore, we investigated the expression of FASN in tissue micro array cohort of 301 DLBCL patients. FASN was found to be expressed in 62.6% (162/259) DLBCL samples and was seen in highly proliferative tumors manifested by high Ki67 (p<0.0001). S

APA, Harvard, Vancouver, ISO, and other styles

24

Yuen, Hiu-Fung, Olga Abramczyk, Grant Montgomery, et al. "Impact of oncogenic driver mutations on feedback between the PI3K and MEK pathways in cancer cells." Bioscience Reports 32, no. 4 (2012): 413–22. http://dx.doi.org/10.1042/bsr20120050.

Full text

Abstract:

Inhibition of the PI3K (phosphoinositide 3-kinase)/Akt/mTORC1 (mammalian target of rapamycin complex 1) and Ras/MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase]/ERK pathways for cancer therapy has been pursued for over a decade with limited success. Emerging data have indicated that only discrete subsets of cancer patients have favourable responses to these inhibitors. This is due to genetic mutations that confer drug insensitivity and compensatory mechanisms. Therefore understanding of the feedback mechanisms that occur with respect to specific

APA, Harvard, Vancouver, ISO, and other styles

25

Yahcoob, Nehla, Baskar Lakshmanan, Jyothi Achuthanandhan, and Vijayakumar Balakrishnan. "In-silico screening of 2,3-diphenylquinozaline derivatives as C-met kinase inhibitors." JOURNAL OF PHARMACEUTICAL CHEMISTRY 4, no. 3 (2017): 41–45. http://dx.doi.org/10.14805/jphchem.2017.art84.

Full text

Abstract:

Quinoxaline, an important class of heterocylic compounds drawn greater attention due to their wide spectrum of biological activities. They are considered as an important chemical scaffold for anticancer drug design due to their potential inhibitory activity against C-met tyrosine kinase. C-met kinase inhibitors are a class of small molecules that having therapeutic potential in the treatment of various types of cancers. The present study aims to focus on the chemistry of quinoxaline derivatives, their potential activities against C-met tyrosine kinase, and in-silico screening of designed compo

APA, Harvard, Vancouver, ISO, and other styles

26

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

27

Xia, Chunlei, Ying Wang, Chen Liu, et al. "Novel Peptide CM 7 Targeted c-Met with Antitumor Activity." Molecules 25, no. 3 (2020): 451. http://dx.doi.org/10.3390/molecules25030451.

Full text

Abstract:

Anomalous changes of the cell mesenchymal–epithelial transition factor (c-Met) receptor tyrosine kinase signaling pathway play an important role in the occurrence and development of human cancers, including gastric cancer. In this study, we designed and synthesized a novel peptide (CM 7) targeting the tyrosine kinase receptor c-Met, that can inhibit c-Met-mediated signaling in MKN-45 and U87 cells. Its affinity to human c-Met protein or c-Met-positive cells was determined, which showed specific binding to c-Met with high affinity. Its biological activities against MKN-45 c-Met-positive cells w

APA, Harvard, Vancouver, ISO, and other styles

28

Huang, Dandan, Xiaoyun Zhu, Chunlei Tang, et al. "3D QSAR Pharmacophore Modeling for c-Met Kinase Inhibitors." Medicinal Chemistry 8, no. 6 (2012): 1117–25. http://dx.doi.org/10.2174/157340612804075142.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Huang, Dandan, Xiaoyun Zhu, Chunlei Tang, et al. "3D QSAR Pharmacophore Modeling for c-Met Kinase Inhibitors." Medicinal Chemistry 8, no. 6 (2012): 1117–25. http://dx.doi.org/10.2174/1573406411208061117.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Giordano, S., C. Ponzetto, M. F. Di Renzo, C. S. Cooper, and P. M. Comoglio. "Tyrosine kinase receptor indistinguishable from the c-met protein." Nature 339, no. 6220 (1989): 155–56. http://dx.doi.org/10.1038/339155a0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Bottaro, DP. "Hepatocyte growth factor, receptor of c-met tyrosine kinase." Biomedicine & Pharmacotherapy 46, no. 8 (1992): 379. http://dx.doi.org/10.1016/0753-3322(92)90313-v.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Zhu, Kongkai, Xiangqian Kong, Dan Zhao, Zhongjie Liang, and Cheng Luo. "c-MET kinase inhibitors: a patent review (2011 – 2013)." Expert Opinion on Therapeutic Patents 24, no. 2 (2013): 217–30. http://dx.doi.org/10.1517/13543776.2014.864279.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Gong, Hua C., Sean Wang, Gary Mayer, et al. "Signatures of Drug Sensitivity in Nonsmall Cell Lung Cancer." International Journal of Proteomics 2011 (August 7, 2011): 1–13. http://dx.doi.org/10.1155/2011/215496.

Full text

Abstract:

We profiled receptor tyrosine kinase pathway activation and key gene mutations in eight human lung tumor cell lines and 50 human lung tumor tissue samples to define molecular pathways. A panel of eight kinase inhibitors was used to determine whether blocking pathway activation affected the tumor cell growth. The HER1 pathway in HER1 mutant cell lines HCC827 and H1975 were found to be highly activated and sensitive to HER1 inhibition. H1993 is a c-MET amplified cell line showing c-MET and HER1 pathway activation and responsiveness to c-MET inhibitor treatment. IGF-1R pathway activated H358 and

APA, Harvard, Vancouver, ISO, and other styles

34

Safaie Qamsari, Elmira, Sepideh Safaei Ghaderi, Bahareh Zarei, et al. "The c-Met receptor: Implication for targeted therapies in colorectal cancer." Tumor Biology 39, no. 5 (2017): 101042831769911. http://dx.doi.org/10.1177/1010428317699118.

Full text

Abstract:

c-Met (mesenchymal–epithelial transition factor) is a tyrosine kinase receptor activated by hepatocyte growth factor and regulates multiple biological processes, such as cell scattering, survival, and proliferation. Aberrant c-Met signaling has been implicated in a variety of cancer types, including colorectal cancer. c-Met is genetically altered through various mechanisms that is associated with colorectal cancer progression and metastasis. Especially, in colorectal cancer, preclinical evidence for the aberrant activation of the c-Met signaling exists. Accordingly, molecular targeting of c-Me

APA, Harvard, Vancouver, ISO, and other styles

35

Zhao, Yutong, Jing Zhao, Rachel K. Mialki, et al. "Lipopolysaccharide-induced phosphorylation of c-Met tyrosine residue 1003 regulates c-Met intracellular trafficking and lung epithelial barrier function." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 1 (2013): L56—L63. http://dx.doi.org/10.1152/ajplung.00417.2012.

Full text

Abstract:

c-Met, the receptor tyrosine kinase whose natural ligand is hepatocyte growth factor, is known to have a key role in cell motility. We have previously shown that lysophosphatidic acid (LPA) induced a decrease in c-Met activation via serine phosphorylation of c-Met at cell-cell contacts. Here, we demonstrate that lipopolysaccharide (LPS) treatment of human bronchial epithelial cells induced internalization of c-Met via phosphorylation at its tyrosine residue 1003. In addition, it induced epithelial barrier dysfunction as evidenced by a decrease in transepithelial resistance (TER) in a time-depe

APA, Harvard, Vancouver, ISO, and other styles

36

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

37

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

38

Passelli, Katiuska, Borja Prat-Luri, Margot Merlot, Michiel Goris, Massimiliano Mazzone, and Fabienne Tacchini-Cottier. "The c-MET receptor tyrosine kinase contributes to neutrophil-driven pathology in cutaneous leishmaniasis." PLOS Pathogens 18, no. 1 (2022): e1010247. http://dx.doi.org/10.1371/journal.ppat.1010247.

Full text

Abstract:

Neutrophils are the first line of defence against invading pathogens. Although neutrophils are well-known professional killers, some pathogens including Leishmania (L.) parasites survive in neutrophils, using these cells to establish infection. Manipulation of neutrophil recruitment to the infection site is therefore of interest in this cutaneous disease. The c-MET tyrosine kinase receptor was shown to promote neutrophil migration to inflamed sites. Here, we investigated the importance of c-MET expression on neutrophils in their recruitment to the infection site and the role of c-Met expressio

APA, Harvard, Vancouver, ISO, and other styles

39

Marrufo-Gallegos, Karla Cecilia, Jose Rafael Villafán-Bernal, Salvador Espino-y-Sosa, et al. "Influential Serum Kinases (Non-sFlt-1) and Phosphatases in Preeclampsia—Systemic Review and Metanalysis." International Journal of Molecular Sciences 24, no. 16 (2023): 12842. http://dx.doi.org/10.3390/ijms241612842.

Full text

Abstract:

The early identification of women with an increased risk of preeclampsia (PE) is desirable, but apart from soluble fms-like tyrosine kinase-1 (sFlt-1), few biomarkers have previously been identified as relevant for predicting preeclampsia. Since kinases and phosphatases regulate critical biological processes and previous evidence suggests a potential role of these molecules in preeclampsia, we performed this systematic review and metanalysis. The objective was to determine if there are kinases and phosphatases whose serum levels are different between women with and without PE, being relevant b

APA, Harvard, Vancouver, ISO, and other styles

40

Dadashpour, Sakineh, Tuba T. Küçükkılınç, Ayse Ercan, Seyed J. Hosseinimehr, Nima Naderi, and Hamid Irannejad. "Synthesis and Anticancer Activity of Benzimidazole/Benzoxazole Substituted Triazolotriazines in Hepatocellular Carcinoma." Anti-Cancer Agents in Medicinal Chemistry 19, no. 17 (2020): 2120–29. http://dx.doi.org/10.2174/1871520619666190808152051.

Full text

Abstract:

Background: Receptor Tyrosine Kinases (RTK) are the main family of cell surface receptors for growth factors, hormones and cytokines which are responsible for cell growth and differentiation and are considered as an important therapeutic target in cancer. Objective: The aim of this study was to design, synthesise and conduct the biological evaluation of benzimidazole/ benzoxazole substituted triazolotriazines as new anticancer agents. Methods: A series of benzimidazolyl and benzoxazolyl-linked triazolotriazines 8a-e and 9a-e were synthesized as receptor tyrosine kinase inhibitors. Target compo

APA, Harvard, Vancouver, ISO, and other styles

41

Kim, Jooseok, Kyung Eui Park, Yoo-Seong Jeong, et al. "Therapeutic Efficacy of ABN401, a Highly Potent and Selective MET Inhibitor, Based on Diagnostic Biomarker Test in MET-Addicted Cancer." Cancers 12, no. 6 (2020): 1575. http://dx.doi.org/10.3390/cancers12061575.

Full text

Abstract:

The receptor tyrosine kinase c-MET regulates processes essential for tissue remodeling and mammalian development. The dysregulation of c-MET signaling plays a role in tumorigenesis. The aberrant activation of c-MET, such as that caused by gene amplification or mutations, is associated with many cancers. c-MET is therefore an attractive therapeutic target, and inhibitors are being tested in clinical trials. However, inappropriate patient selection criteria, such as low amplification or expression level cut-off values, have led to the failure of clinical trials. To include patients who respond t

APA, Harvard, Vancouver, ISO, and other styles

42

Jung, Yang, Kim, et al. "RhoA-Dependent HGF and c-Met Mediate Gas6-Induced Inhibition of Epithelial–Mesenchymal Transition, Migration, and Invasion of Lung Alveolar Epithelial Cells." Biomolecules 9, no. 10 (2019): 565. http://dx.doi.org/10.3390/biom9100565.

Full text

Abstract:

Previously, we demonstrated that growth arrest-specific protein 6 (Gas6)/Axl or Mer signaling inhibited the transforming growth factor (TGF)-β1-induced epithelial–mesenchymal transition (EMT) in lung epithelial cells. Hepatocyte growth factor (HGF) has also been shown to inhibit TGF-β1-induced changes in EMT markers. Here, we examined whether Gas6 signaling can induce the production of HGF and c-Met in lung alveolar epithelial cells to mediate the inhibition of EMT and to inhibit the migration and invasion of epithelial cells. The inhibition of the RhoA/Rho kinase pathway, using either a RhoA-

APA, Harvard, Vancouver, ISO, and other styles

43

Kim, Junyeol, Tae Seung Lee, Myeong Hwan Lee, et al. "Pancreatic Cancer Treatment Targeting the HGF/c-MET Pathway: The MEK Inhibitor Trametinib." Cancers 16, no. 5 (2024): 1056. http://dx.doi.org/10.3390/cancers16051056.

Full text

Abstract:

Pancreatic cancer is characterized by fibrosis/desmoplasia in the tumor microenvironment, which is primarily mediated by pancreatic stellate cells and cancer-associated fibroblasts. HGF/c-MET signaling, which is instrumental in embryonic development and wound healing, is also implicated for its mitogenic and motogenic properties. In pancreatic cancer, this pathway, along with its downstream signaling pathways, is associated with disease progression, prognosis, metastasis, chemoresistance, and other tumor-related factors. Other features of the microenvironment in pancreatic cancer with the HGF/

APA, Harvard, Vancouver, ISO, and other styles

44

Yee, K., TR Bishop, C. Mather, and LI Zon. "Isolation of a novel receptor tyrosine kinase cDNA expressed by developing erythroid progenitors." Blood 82, no. 4 (1993): 1335–43. http://dx.doi.org/10.1182/blood.v82.4.1335.1335.

Full text

Abstract:

Abstract Activation of distinct receptor tyrosine kinases (RTK), such as the products of the c-fms and c-kit proto-oncogenes, profoundly affects hematopoietic development. We have isolated a novel RTK cDNA, called met-related kinase (MRK), which is expressed on early erythroid progenitors. MRK is also expressed in many hematopoietic cell lines, and is not lineage restricted. Several regions within the catalytic domain of MRK have amino acid similarity to the c-met proto-oncogene and v-sea oncogene. Specific polyclonal anti-MRK antisera detects an 84- Kd polypeptide in COS cells transfected wit

APA, Harvard, Vancouver, ISO, and other styles

45

Yee, K., TR Bishop, C. Mather, and LI Zon. "Isolation of a novel receptor tyrosine kinase cDNA expressed by developing erythroid progenitors." Blood 82, no. 4 (1993): 1335–43. http://dx.doi.org/10.1182/blood.v82.4.1335.bloodjournal8241335.

Full text

Abstract:

Activation of distinct receptor tyrosine kinases (RTK), such as the products of the c-fms and c-kit proto-oncogenes, profoundly affects hematopoietic development. We have isolated a novel RTK cDNA, called met-related kinase (MRK), which is expressed on early erythroid progenitors. MRK is also expressed in many hematopoietic cell lines, and is not lineage restricted. Several regions within the catalytic domain of MRK have amino acid similarity to the c-met proto-oncogene and v-sea oncogene. Specific polyclonal anti-MRK antisera detects an 84- Kd polypeptide in COS cells transfected with an expr

APA, Harvard, Vancouver, ISO, and other styles

46

Gisterek, I., R. Matkowski, E. Suder, et al. "Prognostic role of c-met tyrosine kinase receptor expression in breast carcinoma." Journal of Clinical Oncology 24, no. 18_suppl (2006): 10552. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.10552.

Full text

Abstract:

10552 Background: Hepatocyte growth factor is a pleotropic growth factor that regulates cell proliferation, survival, tumor angiogenesis and metastasis. Its biological effects are mediated through interaction with its receptor: c-met protein.In this study, we evaluated c-met expression in the homogenous group of 99 patients diagnosed with stage II ductal breast carcinomas (G2, G3). We analyzed 5 and 10-years overall (OS) and disease free survival (DFS). Methods: Microscopic studies were performed on formalin-fixed, paraffin-embedded tumor tissue, obtained during surgery and stained routinely w

APA, Harvard, Vancouver, ISO, and other styles

47

Ahn, Songyeon, Tagari Samanta, Junhyoung Park, and Benny A. Kaipparettu. "Abstract 5374: Metabolic reprogramming regulates tyrosine receptor kinase c-Met in prostate cancer." Cancer Research 85, no. 8_Supplement_1 (2025): 5374. https://doi.org/10.1158/1538-7445.am2025-5374.

Full text

Abstract:

Mitochondrial metabolic reprogramming is known to regulate oncopathways. To understand mitochondria-regulated oncopathways in prostate cancer (PC), we used a transmitochondrial cybrid system. Under a benign prostate cell line PNT1a, cybrids were generated after cytoplasmic fusion from PNT1a (PNT1/PNT1) and PC cell line PC3 (PC3/PNT1). PC3/PNT1 cybrids showed increased tumor stemness, metastasis, and mitochondrial activity with enhanced OXPHOS and fatty acid oxidation (FAO) compared to PNT1/PNT1 cybrids. RNASeq analysis of cybrids identified increased mRNA expression of Mesenchymal Epithelial T

APA, Harvard, Vancouver, ISO, and other styles

48

Batth, Izhar S., Bijay S. Jaiswal, Dolonchampa Maji, et al. "Abstract 540: c-MET mutations sensitize to antibody-drug conjugate telisotuzumab vedotin through efficient internalization and rapid intracellular drug delivery." Cancer Research 83, no. 7_Supplement (2023): 540. http://dx.doi.org/10.1158/1538-7445.am2023-540.

Full text

Abstract:

Abstract Background: Telisotuzumab vedotin (Teliso-V) is an antibody-drug conjugate (ADC) composed of the c-MET antibody ABT-700 and the microtubule inhibitor monomethyl auristatin E (MMAE). Patients with EGFR wildtype (WT) nonsquamous non-small cell lung cancer with high c-MET expression had an overall response rate of 54% with Teliso-V. In addition to overexpression and amplification, genetic alterations in c-MET, such as exon 14 deletion (ex14del) and missense mutations in the tyrosine kinase domain (TKD), contribute to its constitutive activation. The efficacy of Teliso-V in context of the

APA, Harvard, Vancouver, ISO, and other styles

49

Derman, M. P., M. J. Cunha, E. J. Barros, S. K. Nigam, and L. G. Cantley. "HGF-mediated chemotaxis and tubulogenesis require activation of the phosphatidylinositol 3-kinase." American Journal of Physiology-Renal Physiology 268, no. 6 (1995): F1211—F1217. http://dx.doi.org/10.1152/ajprenal.1995.268.6.f1211.

Full text

Abstract:

The association of hepatocyte growth factor (HGF) with its high-affinity receptor, c-met, has been shown to induce mitogenesis, motogenesis, and morphogenesis in renal epithelial cells (L. G. Cantley, E. J. G. Barros, M. Gandhi, M. Rauchman, and S. K. Nigam. Am. J. Physiol. 267 (Renal Fluid Electrolyte Physiol. 36): F271-F280, 1994), suggesting that HGF may be critical to the orchestration of both renal development and regeneration following injury. Although signal transduction pathways activated by c-met include the phosphatidylinositol 3-kinase (PI-3-kinase), phospholipase C gamma, ras, and

APA, Harvard, Vancouver, ISO, and other styles

50

Li, Gong, Hepeng Shi, Peilong Zhang, et al. "Abstract C145: ANS014004, a novel small-molecule type II c-Met inhibitor effectively overcomes clinical-resistance MET mutations and exhibits antitumor activity in preclinical models of MET-amplified non-small cell lung cancer (NSCLC) and gastric cancer." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): C145. http://dx.doi.org/10.1158/1535-7163.targ-23-c145.

Full text

Abstract:

Abstract Mesenchymal epithelial transition (MET) proto-oncogene receptor tyrosine kinase (RTK) is a cell surface receptor selective for hepatocyte growth factor (HGF), and is involved in embryogenesis regulation, wound healing, organ regeneration, angiogenesis, and immunomodulation. Aberrant MET oncogenic alterations include: MET exon 14 skipping (MET∆ex14) mutations; activating mutations in the kinase domain; MET gene amplification; MET fusions; and MET protein overexpression. These oncogenic alterations occur in a wide range of human solid cancers. Small-molecule type I c-Met inhibitors bind

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!