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Journal articles on the topic 'TGF-β Pathway'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Sopel, Nina, Alexandra Ohs, Mario Schiffer та Janina Müller-Deile. "A Tight Control of Non-Canonical TGF-β Pathways and MicroRNAs Downregulates Nephronectin in Podocytes". Cells 11, № 1 (2022): 149. http://dx.doi.org/10.3390/cells11010149.

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Nephronectin (NPNT) is an extracellular matrix protein in the glomerular basement membrane that is produced by podocytes and is important for the integrity of the glomerular filtration barrier. Upregulated transforming growth factor β (TGF-β) and altered NPNT are seen in different glomerular diseases. TGF-β downregulates NPNT and upregulates NPNT-targeting microRNAs (miRs). However, the pathways involved were previously unknown. By using selective inhibitors of the canonical, SMAD-dependent, and non-canonical TGF-β pathways, we investigated NPNT transcription, translation, secretion, and regul

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Ismaeel, Ahmed, Jeong-Su Kim, Jeffrey S. Kirk, Robert S. Smith, William T. Bohannon та Panagiotis Koutakis. "Role of Transforming Growth Factor-β in Skeletal Muscle Fibrosis: A Review". International Journal of Molecular Sciences 20, № 10 (2019): 2446. http://dx.doi.org/10.3390/ijms20102446.

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Transforming growth factor-beta (TGF-β) isoforms are cytokines involved in a variety of cellular processes, including myofiber repair and regulation of connective tissue formation. Activation of the TGF-β pathway contributes to pathologic fibrosis in most organs. Here, we have focused on examining the evidence demonstrating the involvement of TGF-β in the fibrosis of skeletal muscle particularly. The TGF-β pathway plays a role in different skeletal muscle myopathies, and TGF-β signaling is highly induced in these diseases. In this review, we discuss different molecular mechanisms of TGF-β-medi

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Li, Yuchao, Difan Deng, Chris Tina Höfer та ін. "Liebig’s law of the minimum in the TGF-β/SMAD pathway". PLOS Computational Biology 20, № 5 (2024): e1012072. http://dx.doi.org/10.1371/journal.pcbi.1012072.

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Cells use signaling pathways to sense and respond to their environments. The transforming growth factor-β (TGF-β) pathway produces context-specific responses. Here, we combined modeling and experimental analysis to study the dependence of the output of the TGF-β pathway on the abundance of signaling molecules in the pathway. We showed that the TGF-β pathway processes the variation of TGF-β receptor abundance using Liebig’s law of the minimum, meaning that the output-modifying factor is the signaling protein that is most limited, to determine signaling responses across cell types and in single

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Moradi-Marjaneh, Reyhaneh, Majid Khazaei, Gordon A. Ferns та Seyed H. Aghaee-Bakhtiari. "The Role of TGF-β Signaling Regulatory MicroRNAs in the Pathogenesis of Colorectal Cancer". Current Pharmaceutical Design 24, № 39 (2019): 4611–18. http://dx.doi.org/10.2174/1381612825666190110150705.

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Colorectal cancer (CRC) is one of the most common cancers globally and is associated with a high mortality rate. The transforming growth factor beta (TGF-β) signaling pathway plays an important role in normal intestinal tissue function, but has also been implicated in the development of CRC. MicroRNAs (miRNAs) have also recently emerged as important regulators of cancer development and progression. They act by targeting multiple signaling pathways including the TGF-β signaling pathway. There is growing evidence demonstrating that miRNAs target various components of the TGF-β signaling pathway,

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Elliott, Rebecca L., and Gerard C. Blobe. "Role of Transforming Growth Factor Beta in Human Cancer." Journal of Clinical Oncology 23, no. 9 (2005): 2078–93. http://dx.doi.org/10.1200/jco.2005.02.047.

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Transforming growth factor beta (TGF-β) is a ubiquitous and essential regulator of cellular and physiologic processes including proliferation, differentiation, migration, cell survival, angiogenesis, and immunosurveillance. Alterations in the TGF-β signaling pathway, including mutation or deletion of members of the signaling pathway and resistance to TGF-β-mediated inhibition of proliferation are frequently observed in human cancers. Although these alterations define a tumor suppressor role for the TGF-β pathway in human cancer, TGF-β also mediates tumor-promoting effects, either through diffe

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Lamouille, Samy, та Rik Derynck. "Cell size and invasion in TGF-β–induced epithelial to mesenchymal transition is regulated by activation of the mTOR pathway". Journal of Cell Biology 178, № 3 (2007): 437–51. http://dx.doi.org/10.1083/jcb.200611146.

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Epithelial to mesenchymal transition (EMT) occurs during development and cancer progression to metastasis and results in enhanced cell motility and invasion. Transforming growth factor-β (TGF-β) induces EMT through Smads, leading to transcriptional regulation, and through non-Smad pathways. We observe that TGF-β induces increased cell size and protein content during EMT. This translational regulation results from activation by TGF-β of mammalian target of rapamycin (mTOR) through phosphatidylinositol 3-kinase and Akt, leading to the phosphorylation of S6 kinase 1 and eukaryotic initiation fact

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Nlandu Khodo, Stellor, Surekha Neelisetty, Luke Woodbury та ін. "Deleting the TGF-β receptor in proximal tubules impairs HGF signaling". American Journal of Physiology-Renal Physiology 310, № 6 (2016): F499—F510. http://dx.doi.org/10.1152/ajprenal.00446.2015.

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Transforming growth factor-β (TGF-β) and hepatocyte growth factor (HGF) play key roles in regulating the response to renal injury but are thought to mediate divergent effects on cell behavior. However, how TGF-β signaling alters the response to HGF in epithelia, the key site of HGF signaling in the injured kidney, is not well studied. Contrary to our expectation, we showed that deletion of the TGF-β type II receptor in conditionally immortalized proximal tubule (PT) cells impaired HGF-dependent signaling. This reduced signaling was due to decreased transcription of c-Met, the HGF receptor, and

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Dong, Mei, та Gerard C. Blobe. "Role of transforming growth factor-β in hematologic malignancies". Blood 107, № 12 (2006): 4589–96. http://dx.doi.org/10.1182/blood-2005-10-4169.

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AbstractThe transforming growth factor-β (TGF-β) signaling pathway is an essential regulator of cellular processes, including proliferation, differentiation, migration, and cell survival. During hematopoiesis, the TGF-β signaling pathway is a potent negative regulator of proliferation while stimulating differentiation and apoptosis when appropriate. In hematologic malignancies, including leukemias, myeloproliferative disorders, lymphomas, and multiple myeloma, resistance to these homeostatic effects of TGF-β develops. Mechanisms for this resistance include mutation or deletion of members of th

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García-Sánchez, Omar, Sandra M. Sancho-Martínez, José Miguel López-Novoa та Francisco J. López-Hernández. "Activation of the ALK-5 Pathway is not per se Sufficient for the Antiproliferative Effect of TGF-β1 on Renal Tubule Epithelial Cells". Cellular Physiology and Biochemistry 37, № 4 (2015): 1231–39. http://dx.doi.org/10.1159/000430246.

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Background/Aims: Defective tissue repair underlies renal tissue degeneration during chronic kidney disease (CKD) progression. Unbalanced presence of TGF-β opposes effective cell proliferation and differentiation processes, necessary to replace damaged epithelia. TGF-β also retains arrested cells in a fibrotic phenotype responsible for irreversible scarring. In order to identify prospective molecular targets to prevent the effect of TGF-β during CKD, we studied the signaling pathways responsible for the antiproliferative effect of this cytokine. Methods: Tubule epithelial HK2 and MDCK cells wer

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Jayaraman, Selvaraj. "Molecular docking analysis of imiquimod with the TGF-β targets for oral carcinoma". Bioinformation 19, № 4 (2023): 467–70. http://dx.doi.org/10.6026/97320630019467.

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TGF-β signalling pathway is the main signalling pathways that regulate various biological functions such as cell proliferation, apoptosis, metabolic dysregulation, and metastasis in many cancer cells. Previous studies have elaborated the role of TGF-β signalling targets have a significant regulatory function in various cancers. Moreover targeting the epithelial to mesenchymal transition markers in oral squamous cell carcinoma not yet elucidated. Therefore, it is of interest to document the molecular docking analysis of TGF-β signalling pathway targets such as Smad2, GATA2 and MAFG with imiquim

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Mangani, Davide, Michael Weller, Emad Seyed Sadr та ін. "Limited role for transforming growth factor–β pathway activation-mediated escape from VEGF inhibition in murine glioma models". Neuro-Oncology 18, № 12 (2016): 1610–21. http://dx.doi.org/10.1093/neuonc/now112.

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AbstractBackgroundThe vascular endothelial growth factor (VEGF) and transforming growth factor (TGF)–β pathways regulate key biological features of glioblastoma. Here we explore whether the TGF-β pathway, which promotes angiogenesis, invasiveness, and immunosuppression, acts as an escape pathway from VEGF inhibition.MethodsThe role of the TGF-β pathway in escape from VEGF inhibition was assessed in vitro and in vivo and by gene expression profiling in syngeneic mouse glioma models.ResultsWe found that TGF-β is an upstream regulator of VEGF, whereas VEGF pathway activity does not alter the TGF-

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Niimi, Hideki, Katerina Pardali, Michael Vanlandewijck, Carl-Henrik Heldin та Aristidis Moustakas. "Notch signaling is necessary for epithelial growth arrest by TGF-β". Journal of Cell Biology 176, № 5 (2007): 695–707. http://dx.doi.org/10.1083/jcb.200612129.

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Transforming growth factor β (TGF-β) and Notch act as tumor suppressors by inhibiting epithelial cell proliferation. TGF-β additionally promotes tumor invasiveness and metastasis, whereas Notch supports oncogenic growth. We demonstrate that TGF-β and ectopic Notch1 receptor cooperatively arrest epithelial growth, whereas endogenous Notch signaling was found to be required for TGF-β to elicit cytostasis. Transcriptomic analysis after blocking endogenous Notch signaling uncovered several genes, including Notch pathway components and cell cycle and apoptosis factors, whose regulation by TGF-β req

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Zhang, Haojian, David Kozono, Kevin O'Connor та ін. "Bone Marrow Failure in Fanconi Anemia from Hyperactive TGF-β Signaling". Blood 124, № 21 (2014): 356. http://dx.doi.org/10.1182/blood.v124.21.356.356.

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Abstract Fanconi anemia (FA) is the most common inherited bone marrow failure syndrome. FA patients develop bone marrow failure during the first decade of life due to attrition of hematopoietic stem and progenitor cells (HSPCs). FA patients also develop other hematologic manifestations, including myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) due to clonal evolution. FA is caused by biallelic mutants in one of sixteen FANC genes, the products of which cooperate in the FA/BRCA DNA repair pathway and regulate cellular resistance to DNA cross-linking agents. Bone marrow failure i

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Tian, Bole, Mao Li, Dan Cao та ін. "Alteration of TGF-β signaling pathway predicts worse prognosis in pancreatic ductal adenocarcinoma." Journal of Clinical Oncology 37, № 15_suppl (2019): e13006-e13006. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e13006.

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e13006 Background: Transforming growth factor beta (TGF-β) signaling pathway is one of the core pathways involved in tumor initiation and progression. The prognostic value of TGF-β pathway genes as a functionally related group in pancreatic ductal adenocarcinoma (PDAC) is rarely studied. Methods: 72 PDAC patients who underwent surgery between November 30, 2015 and September 13, 2017 in West China Hospital, Sichuan University were identified and included in this study. Whole-exome sequencing (WES) or targeted next-generation sequencing was performed with tumor tissue from all the participants.

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Kollias, Helen D., та John C. McDermott. "Transforming growth factor-β and myostatin signaling in skeletal muscle". Journal of Applied Physiology 104, № 3 (2008): 579–87. http://dx.doi.org/10.1152/japplphysiol.01091.2007.

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The superfamily of transforming growth factor-β (TGF-β) cytokines has been shown to have profound effects on cellular proliferation, differentiation, and growth. Recently, there have been major advances in our understanding of the signaling pathway(s) conveying TGF-β signals to the nucleus to ultimately control gene expression. One tissue that is potently influenced by TGF-β superfamily signaling is skeletal muscle. Skeletal muscle ontogeny and postnatal physiology have proven to be exquisitely sensitive to the TGF-β superfamily cytokine milieu in various animal systems from mice to humans. Re

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Wu, Tingting, Bingqian Liu, Yongjie Wei та Zhigang Li. "TGF-β Regulates m6A RNA Methylation after PM2.5 Exposure". Toxics 11, № 12 (2023): 1026. http://dx.doi.org/10.3390/toxics11121026.

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PM2.5 exposure leads to a variety of respiratory diseases, including pulmonary fibrosis, metastatic lung cancer, etc. Exposure to PM2.5 results in the alteration of epigenetic modification. M6A RNA methylation is an essential epigenetic modification that regulates gene expression at the post-transcriptional level. Our previous study found that PM2.5 exposure up-regulated m6A RNA methylation and TGF-β expression level in the lung, but the mechanisms and pathways of PM2.5 regulation of m6A RNA methylation are still unclear. Moreover, a previous study reported that the TGF-β signal pathway could

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Fernandez, Tania, Stephanie Amoroso, Shellyann Sharpe та ін. "Disruption of Transforming Growth Factor β Signaling by a Novel Ligand-dependent Mechanism". Journal of Experimental Medicine 195, № 10 (2002): 1247–55. http://dx.doi.org/10.1084/jem.20011521.

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Transforming growth factor (TGF)-β is the prototype in a family of secreted proteins that act in autocrine and paracrine pathways to regulate cell development and function. Normal cells typically coexpress TGF-β receptors and one or more isoforms of TGF-β, thus the synthesis and secretion of TGF-β as an inactive latent complex is considered an essential step in regula-ting the activity of this pathway. To determine whether intracellular activation of TGF-β results in TGF-β ligand–receptor interactions within the cell, we studied pristane-induced plasma cell tumors (PCTs). We now demonstrate th

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He, Changhuai, Pin Ye, Xuecheng Zhang та ін. "The Role of TGF-β Signaling in Saphenous Vein Graft Failure after Peripheral Arterial Disease Bypass Surgery". International Journal of Molecular Sciences 24, № 12 (2023): 10381. http://dx.doi.org/10.3390/ijms241210381.

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Saphenous vein bypass grafting is an effective technique used to treat peripheral arterial disease (PAD). However, restenosis is the major clinical challenge for the graft vessel among people with PAD postoperation. We hypothesize that there is a common culprit behind arterial occlusion and graft restenosis. To investigate this hypothesis, we found TGF-β, a gene specifically upregulated in PAD arteries, by bioinformatics analysis. TGF-β has a wide range of biological activities and plays an important role in vascular remodeling. We discuss the molecular pathway of TGF-β and elucidate its mecha

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Zhao, Yiyang, Linkang He, Tian Wang, Lifang Zhu та Nianlong Yan. "2-Hydroxypropyl-β-cyclodextrin Regulates the Epithelial to Mesenchymal Transition in Breast Cancer Cells by Modulating Cholesterol Homeostasis and Endoplasmic Reticulum Stress". Metabolites 11, № 8 (2021): 562. http://dx.doi.org/10.3390/metabo11080562.

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Cholesterol metabolism affects endoplasmic reticulum (ER) stress and modulates epithelial-mesenchymal transition (EMT). Our previous study demonstrated that 2-hydroxypropyl-β-cyclodextrin (HP-β-CD) attenuated EMT by blocking the transforming growth factor (TGF)-β/Smad signaling pathway and activating ER stress in MDA-MB-231 cells. To further assess the detailed mechanisms between cholesterol metabolism, ER stress, and EMT, LXR-623 (an agonist of LXRα) and simvastatin were used to increase and decrease cholesterol efflux and synthesis, respectively. Here, we found that high HP-β-CD concentratio

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Xu, Yiru, Siliang Xue, Jin Zhou, John J. Voorhees та Gary J. Fisher. "Notch and TGF-β pathways cooperatively regulate receptor protein tyrosine phosphatase-κ (PTPRK) gene expression in human primary keratinocytes". Molecular Biology of the Cell 26, № 6 (2015): 1199–206. http://dx.doi.org/10.1091/mbc.e14-12-1591.

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Receptor protein tyrosine phosphatase-κ (PTPRK) specifically and directly dephosphorylates epidermal growth factor receptor (EGFR), thereby limiting EGFR function in primary human keratinocytes. PTPRK expression is increased by the TGF-β/Smad3 pathway and cell–cell contact. Because the Notch receptor pathway is responsive to cell–cell contact and regulates keratinocyte growth and differentiation, we investigated the interplay between Notch and TGF-β pathways in regulation of PTPRK expression in human keratinocytes. Suppression of Notch signaling by γ-secretase inhibitors substantially reduced

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Her, Kyu Hee. "Transforming Growth Factor-β signaling on tumorigenesis". Journal of Medicine and Life Science 4, № 1 (2006): 21–39. http://dx.doi.org/10.22730/jmls.2006.4.1.21.

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Transforming growth factor beta (TGF-β ) is a ubiquitous multifunctional polypetide and essential regulator of cellular and physiologic processes including proliferation, differentiation, adhesion, migration, apoptosis, angiogenesis and immunosurveillance. Abnormal activation or inhibition of these TGF-β signaling pathway, including mutation or deletion of members of the signaling pathway and resistance to TGF-β -mediated inhibition of proliferation are frequently observed in human cancers. Although these alterations define a tumor suppressor role for the TGF-β pathway in human cancer, TGF-β a

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Marincola Smith, Paula, Anna Means та R. Beauchamp. "Immunomodulatory Effects of TGF-β Family Signaling within Intestinal Epithelial Cells and Carcinomas". Gastrointestinal Disorders 1, № 2 (2019): 290–300. http://dx.doi.org/10.3390/gidisord1020024.

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TGF-β superfamily signaling is responsible for many critical cellular functions including control of cell growth, cell proliferation, cell differentiation, and apoptosis. TGF-β appears to be critical in gastrulation, embryonic development, and morphogenesis, and it retains pleiotropic roles in many adult tissues and cell types in a highly context-dependent manner. While TGF-β signaling within leukocytes is known to have an immunosuppressive role, its immunomodulatory effects within epithelial cells and epithelial cancers is less well understood. Recent data has emerged that suggests TGF-β path

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Sokol, Jonathan P., та William P. Schiemann. "Cystatin C Antagonizes Transforming Growth Factor β Signaling in Normal and Cancer Cells". Molecular Cancer Research 2, № 3 (2004): 183–95. http://dx.doi.org/10.1158/1541-7786.183.2.3.

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Abstract Cystatin C (CystC) is a secreted cysteine protease inhibitor that regulates bone resorption, neutrophil chemotaxis, and tissue inflammation, as well as resistance to bacterial and viral infections. CystC is ubiquitously expressed and present in most bodily fluids where it inhibits the activities of cathepsins, a family of cysteine proteases that can promote cancer cell invasion and metastasis. Transforming growth factor β (TGF-β) is a multifunctional cytokine endowed with both tumor-suppressing and tumor-promoting activities. We show herein that TGF-β treatment up-regulated CystC tran

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de Lucas, María Pilar, Marta Jiménez, Paloma Sánchez-Pavón, Alberto G. Sáez та Encarnación Lozano. "SMA-10 Is a Non-Canonical Member of the TGF-β Sma/Mab Pathway and Immunity Regulator via the DAF-2 Insulin Receptor in Caenorhabditis elegans". International Journal of Molecular Sciences 22, № 2 (2021): 638. http://dx.doi.org/10.3390/ijms22020638.

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Transforming growth factor β (TGF-β) signalling pathways are highly conserved across metazoa and play essential roles not only during development but also in adult tissue maintenance. Alterations of these pathways usually result in a plethora of pathologies. In the nematode Caenorhabditis elegans, the TGF-β Sma/Mab (small/male abnormal) pathway regulates various worm phenotypes such as body size, immune response, ageing, matricide and reproductive span. SMA-10 has been described as a positive modulator of worm body size through the TGF-β Sma/Mab pathway. To better understand if SMA-10 is a cor

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de Lucas, María Pilar, Marta Jiménez, Paloma Sánchez-Pavón, Alberto G. Sáez та Encarnación Lozano. "SMA-10 Is a Non-Canonical Member of the TGF-β Sma/Mab Pathway and Immunity Regulator via the DAF-2 Insulin Receptor in Caenorhabditis elegans". International Journal of Molecular Sciences 22, № 2 (2021): 638. http://dx.doi.org/10.3390/ijms22020638.

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Transforming growth factor β (TGF-β) signalling pathways are highly conserved across metazoa and play essential roles not only during development but also in adult tissue maintenance. Alterations of these pathways usually result in a plethora of pathologies. In the nematode Caenorhabditis elegans, the TGF-β Sma/Mab (small/male abnormal) pathway regulates various worm phenotypes such as body size, immune response, ageing, matricide and reproductive span. SMA-10 has been described as a positive modulator of worm body size through the TGF-β Sma/Mab pathway. To better understand if SMA-10 is a cor

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Kuznetsova, Alla V., Olga P. Popova, Tamara I. Danilova, Andrey V. Latyshev, Oleg O. Yanushevich та Alexey A. Ivanov. "Effects of ECM Components on Periodontal Ligament Stem Cell Differentiation Under Conditions of Disruption of Wnt and TGF-β Signaling Pathways". Journal of Functional Biomaterials 16, № 3 (2025): 94. https://doi.org/10.3390/jfb16030094.

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Periodontitis is accompanied by inflammation that causes dysregulation of the Wnt/β-catenin and TGF-β signaling pathways. This leads to a violation of the homeostasis of periodontal tissues. Components of the extracellular matrix (ECM) are an important part of biomaterials used for the repair of periodontal tissue. The purpose of this study was to evaluate the components of the effect of ECM (hyaluronic acid (HA), fibronectin (Fn), and laminin (Lam)) on the osteogenic and odontogenic differentiation of periodontal ligament stem cells (PDLSCs) in the collagen I hydrogel under conditions of disr

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Madala, Satish K., Thomas R. Korfhagen, Stephanie Schmidt та ін. "Inhibition of the αvβ6 integrin leads to limited alteration of TGF-α-induced pulmonary fibrosis". American Journal of Physiology-Lung Cellular and Molecular Physiology 306, № 8 (2014): L726—L735. http://dx.doi.org/10.1152/ajplung.00357.2013.

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A number of growth factors and signaling pathways regulate matrix deposition and fibroblast proliferation in the lung. The epidermal growth factor receptor (EGFR) family of receptors and the transforming growth factor-β (TGF-β) family are active in diverse biological processes and are central mediators in the initiation and maintenance of fibrosis in many diseases. Transforming growth factor-α (TGF-α) is a ligand for the EGFR, and doxycycline (Dox)-inducible transgenic mice conditionally expressing TGF-α specifically in the lung epithelium develop progressive fibrosis accompanied with cachexia

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Gachpazan, Meysam, Hoda Kashani, Seyed M. Hassanian, et al. "Therapeutic Potential of Targeting Transforming Growth Factor-beta in Colorectal Cancer: Rational and Progress." Current Pharmaceutical Design 25, no. 38 (2019): 4085–89. http://dx.doi.org/10.2174/1381612825666191105114539.

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Background: Colorectal cancer (CRC) is one of the most common types of cancer and is associated with an increasing rate of mortality. Transforming Growth Factor-Beta (TGF-β) is often upregulated in CRC, and appears to play an important role in regulating cell proliferation, migration, immune surveillance, apoptosis, cell differentiation, drug-resistance and many cellular processes that may be involved in CRC, and therefore underscores its potential value as a therapeutic target in the treatment of CRC. An increased expression of the TGF- β pathway has been associated with poor prognosis in sev

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Johnson, Aaron N., та Stuart J. Newfeld. "The TGF-β Family: Signaling Pathways, Developmental Roles, and Tumor Suppressor Activities". Scientific World JOURNAL 2 (2002): 892–925. http://dx.doi.org/10.1100/tsw.2002.178.

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Intercellular communication is a critical process for all multicellular organisms, and communication among cells is required for proper embryonic development and adult physiology. Members of the Transforming Growth Factor-β (TGF-β) family of secreted proteins communicate information between cells via a complex signaling pathway, and family members are capable of inducing a wide range of cellular responses. The purpose of this review is to provide the reader with a broad introduction to our current understanding of three aspects of the TGF-β family. These are the molecular mechanisms utilized b

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Zhang, Xianglan, Jun Seop Yun, Dawool Han, Jong In Yook, Hyun Sil Kim та Eunae Sandra Cho. "TGF-β Pathway in Salivary Gland Fibrosis". International Journal of Molecular Sciences 21, № 23 (2020): 9138. http://dx.doi.org/10.3390/ijms21239138.

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Fibrosis is presented in various physiologic and pathologic conditions of the salivary gland. Transforming growth factor beta (TGF-β) pathway has a pivotal role in the pathogenesis of fibrosis in several organs, including the salivary glands. Among the TGF-β superfamily members, TGF-β1 and 2 are pro-fibrotic ligands, whereas TGF-β3 and some bone morphogenetic proteins (BMPs) are anti-fibrotic ligands. TGF-β1 is thought to be associated with the pro-fibrotic pathogenesis of sialadenitis, post-radiation salivary gland dysfunction, and Sjögren’s syndrome. Potential therapeutic strategies that tar

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Gonzalez-Sanchez, Ester, Javier Vaquero, Maite G. Férnandez-Barrena та ін. "The TGF-β Pathway: A Pharmacological Target in Hepatocellular Carcinoma?" Cancers 13, № 13 (2021): 3248. http://dx.doi.org/10.3390/cancers13133248.

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Transforming Growth Factor-beta (TGF-β) superfamily members are essential for tissue homeostasis and consequently, dysregulation of their signaling pathways contributes to the development of human diseases. In the liver, TGF-β signaling participates in all the stages of disease progression from initial liver injury to hepatocellular carcinoma (HCC). During liver carcinogenesis, TGF-β plays a dual role on the malignant cell, behaving as a suppressor factor at early stages, but contributing to later tumor progression once cells escape from its cytostatic effects. Moreover, TGF-β can modulate the

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Li, Chia-Jung, Pei-Yi Chu, Giou-Teng Yiang, and Meng-Yu Wu. "The Molecular Mechanism of Epithelial–Mesenchymal Transition for Breast Carcinogenesis." Biomolecules 9, no. 9 (2019): 476. http://dx.doi.org/10.3390/biom9090476.

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The transforming growth factor-β (TGF-β) signaling pathway plays multiple regulatory roles in the tumorigenesis and development of cancer. TGF-β can inhibit the growth and proliferation of epithelial cells and induce apoptosis, thereby playing a role in inhibiting breast cancer. Therefore, the loss of response in epithelial cells that leads to the inhibition of cell proliferation due to TGF-β is a landmark event in tumorigenesis. As tumors progress, TGF-β can promote tumor cell invasion, metastasis, and drug resistance. At present, the above-mentioned role of TGF-β is related to the interactio

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Kukes, Vladimir G., Alexey B. Prokofiev, Olga K. Parfenova, et al. "Role of transforming growth factor beta in tumor process." Человек и его здоровье 24, no. 3 (2021): 61–69. http://dx.doi.org/10.21626/vestnik/2021-3/07.

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The study and application of representatives of the transforming growth factor-beta (TGF-β) family in practical medicine remains an urgent task at the present time. A more detailed study of the properties and activity of proteins related to TGF-β opens up new possibilities in the treatment and diagnosis of diseases associated with skeletal muscles, female reproductive system, oncology and the cardiovascular system, as well as in the development of drugs based on them. This work examines the role of TGF-β in tumor development and the potential of this protein as a therapeutic target, as well as

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Ashrafizadeh, Milad, Masoud Najafi, Sima Orouei та ін. "Resveratrol Modulates Transforming Growth Factor-Beta (TGF-β) Signaling Pathway for Disease Therapy: A New Insight into Its Pharmacological Activities". Biomedicines 8, № 8 (2020): 261. http://dx.doi.org/10.3390/biomedicines8080261.

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Resveratrol (Res) is a well-known natural product that can exhibit important pharmacological activities such as antioxidant, anti-diabetes, anti-tumor, and anti-inflammatory. An evaluation of its therapeutic effects demonstrates that this naturally occurring bioactive compound can target different molecular pathways to exert its pharmacological actions. Transforming growth factor-beta (TGF-β) is an important molecular pathway that is capable of regulating different cellular mechanisms such as proliferation, migration, and angiogenesis. TGF-β has been reported to be involved in the development

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Pan, Qiaowei, Tomas Kay, Alexandra Depincé та ін. "Evolution of master sex determiners: TGF-β signalling pathways at regulatory crossroads". Philosophical Transactions of the Royal Society B: Biological Sciences 376, № 1832 (2021): 20200091. http://dx.doi.org/10.1098/rstb.2020.0091.

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To date, more than 20 different vertebrate master sex-determining genes have been identified on different sex chromosomes of mammals, birds, frogs and fish. Interestingly, six of these genes are transcription factors ( Dmrt1 - or Sox3 - related) and 13 others belong to the TGF-β signalling pathway ( Amh , Amhr2 , Bmpr1b , Gsdf and Gdf6 ). This pattern suggests that only a limited group of factors/signalling pathways are prone to become top regulators again and again. Although being clearly a subordinate member of the sex-regulatory network in mammals, the TGF-β signalling pathway made it to th

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Blokzijl, Andries, Camilla Dahlqvist, Eva Reissmann та ін. "Cross-talk between the Notch and TGF-β signaling pathways mediated by interaction of the Notch intracellular domain with Smad3". Journal of Cell Biology 163, № 4 (2003): 723–28. http://dx.doi.org/10.1083/jcb.200305112.

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The Notch and transforming growth factor-β (TGF-β) signaling pathways play critical roles in the control of cell fate during metazoan development. However, mechanisms of cross-talk and signal integration between the two systems are unknown. Here, we demonstrate a functional synergism between Notch and TGF-β signaling in the regulation of Hes-1, a direct target of the Notch pathway. Activation of TGF-β signaling up-regulated Hes-1 expression in vitro and in vivo. This effect was abrogated in myogenic cells by a dominant-negative form of CSL, an essential DNA-binding component of the Notch pathw

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Lee, H. R., R. E. Go та K. C. Choi. "127 TREATMENTS WITH DIVERSE ENDOCRINE-DISRUPTING CHEMICALS RESULTED IN THE INHIBITION OF OVARIAN TUMOR PROGRESSION VIA INTERRUPTION OF TRANSFORMING GROWTH FACTOR-β IN IN VITRO AND XENOGRAFTED MOUSE MODELS". Reproduction, Fertility and Development 26, № 1 (2014): 177. http://dx.doi.org/10.1071/rdv26n1ab127.

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Activated oestrogen receptor (ER) signaling pathway by 17β-estadiol (E2) appeared to suppress transforming growth factor β (TGF-β) signaling pathway by cross-talk with TGF-β components in ER-positive cancer cells. In this study, we further examined the inhibitory effects of alkylphenols, including 4-nonylphenol (NP), 4-otylphenol (OP), bisphenol A (BPA), and benzophenon-1 (BP-1), in TGF-β signaling pathway. The transcriptional and translational levels of TGF-β-related genes were examined by reverse-transcription PCR (RT-PCR), Western blotting analysis in xenografted mouse models of ovarian can

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Huang, Jennifer J., та Gerard C. Blobe. "Dichotomous roles of TGF-β in human cancer". Biochemical Society Transactions 44, № 5 (2016): 1441–54. http://dx.doi.org/10.1042/bst20160065.

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Transforming growth factor-β (TGF-β) mediates numerous biological processes, including embryonic development and the maintenance of cellular homeostasis in a context-dependent manner. Consistent with its central role in maintaining cellular homeostasis, inhibition of TGF-β signaling results in disruption of normal homeostatic processes and subsequent carcinogenesis, defining the TGF-β signaling pathway as a tumor suppressor. However, once carcinogenesis is initiated, the TGF-β signaling pathway promotes cancer progression. This dichotomous function of the TGF-β signaling pathway is mediated th

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Wang, Xiao-Ling, Meng Yang та Ying Wang. "Roles of transforming growth factor-β signaling in liver disease". World Journal of Hepatology 16, № 7 (2024): 973–79. http://dx.doi.org/10.4254/wjh.v16.i7.973.

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In this editorial we expand the discussion on the article by Zhang et al published in the recent issue of the World Journal of Hepatology . We focus on the diagnostic and therapeutic targets identified on the basis of the current understanding of the molecular mechanisms of liver disease. Transforming growth factor-β (TGF-β) belongs to a structurally related cytokine super family. The family members display different time- and tissue-specific expression patterns associated with autoimmunity, inflammation, fibrosis, and tumorigenesis; and, they participate in the pathogenesis of many diseases.

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Kim, Min Soo, та Wook Jin. "TrkB-Induced Inhibition of R-SMAD/SMAD4 Activation is Essential for TGF-β-Mediated Tumor Suppressor Activity". Cancers 12, № 4 (2020): 1048. http://dx.doi.org/10.3390/cancers12041048.

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TrkB-mediated activation of the IL6/JAK2/STAT3 signaling pathway is associated with the induction of the epithelial–mesenchymal transition (EMT) program and the acquisition of metastatic potential by tumors. Conversely, the transforming of growth factor-β (TGF-β) is implicated in tumor suppression through the canonical SMAD-dependent signaling pathway. Hence, TrkB could play a role in disrupting the potent TGF-β-mediated growth inhibition, a concept that has not been fully explored. Here, we identified TrkB to be a crucial regulator of the TGF-β signaling pathway as it inhibits the TGF-β-media

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Kucuksayan, Hakan, Sakir Akgun, Osman Nidai Ozes та ін. "TGF-β–SMAD–miR-520e axis regulates NSCLC metastasis through a TGFBR2-mediated negative-feedback loop". Carcinogenesis 40, № 5 (2018): 695–705. http://dx.doi.org/10.1093/carcin/bgy166.

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Abstract Transforming growth factor-β (TGF-β) pathway plays crucial roles during the carcinogenesis and metastasis. TGF-β receptor 2 (TGFBR2) is a key molecule for the regulation of TGF-β pathway and frequently downregulated or lost in several cancer types including non-small cell lung cancer (NSCLC), and TGF-β pathway is often regulated by negative-feedback mechanisms, but little is known about the mechanism of TGFBR2 downregulation in NSCLC. Here, we found that the expression of miR-520e is upregulated in metastatic tumor tissues compared with non-metastatic ones, and its expression is inver

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Schnaper, H. William, Tomoko Hayashida, Susan C. Hubchak та Anne-Christine Poncelet. "TGF-β signal transduction and mesangial cell fibrogenesis". American Journal of Physiology-Renal Physiology 284, № 2 (2003): F243—F252. http://dx.doi.org/10.1152/ajprenal.00300.2002.

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Transforming growth factor-β (TGF-β) is closely associated with progressive renal fibrosis. Significant progress has been accomplished in determining the cellular signaling pathways that are activated by TGF-β. This knowledge is being applied to glomerular mesangial cell models of extracellular matrix (ECM) accumulation. A central component of TGF-β-stimulated mesangial cell fibrogenesis is the TGF-β family-specific Smad signal transduction pathway. However, while Smads play an important role in collagen accumulation, recent findings indicate that cross talk among a variety of pathways is nece

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Yan, Xiaohua, та Ye-Guang Chen. "Smad7: not only a regulator, but also a cross-talk mediator of TGF-β signalling". Biochemical Journal 434, № 1 (2011): 1–10. http://dx.doi.org/10.1042/bj20101827.

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TGF-β (transforming growth factor-β) is a pleiotropic cytokine regulating diverse cellular processes. It signals through membrane-bound receptors, downstream Smad proteins and/or other signalling mediators. Smad7 has been well established to be a key negative regulator of TGF-β signalling. It antagonizes TGF-β signalling through multiple mechanisms in the cytoplasm and in the nucleus. Smad7 can be transcriptionally induced by TGF-β and other growth factors and serves as an important cross-talk mediator of the TGF-β signalling pathway with other signalling pathways. Accordingly, it plays pivota

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Iyer, Abhirami Kannan, Jennifer C. Bailey, Renukaradhya Gourapura, Yinling Lin, Hoa B. Nguyen та Randy Brutkiewicz. "Inhibition of CD1d-mediated antigen presentation by the TGF-β/Smad signaling pathway (APP3P.113)". Journal of Immunology 192, № 1_Supplement (2014): 111.14. http://dx.doi.org/10.4049/jimmunol.192.supp.111.14.

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Abstract CD1d is a MHC class I-like molecule that presents lipid Ags to a subpopulation of innate lymphocytes called natural killer T cells. In a prior study, we showed that the mitogen-activated protein kinase p38 is a negative regulator of Ag presentation by CD1d. It is unknown how p38 is activated to induce this regulation; however, several studies have implicated a role for the immunoregulatory cytokine, TGF-β, in the activation of p38. Therefore, we hypothesized that TGF-β negatively regulates the CD1d-mediated Ag presentation pathway. Indeed, a dose-dependent decrease in CD1d-mediated Ag

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Gungor, Medine Zeynep, Merve Uysal та Serif Senturk. "The Bright and the Dark Side of TGF-β Signaling in Hepatocellular Carcinoma: Mechanisms, Dysregulation, and Therapeutic Implications". Cancers 14, № 4 (2022): 940. http://dx.doi.org/10.3390/cancers14040940.

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Hepatocellular carcinoma (HCC) is associated with genetic and nongenetic aberrations that impact multiple genes and pathways, including the frequently dysregulated transforming growth factor β (TGF-β) signaling pathway. The regulatory cytokine TGF-β and its signaling effectors govern a broad spectrum of spatiotemporally regulated molecular and cellular responses, yet paradoxically have dual and opposing roles in HCC progression. In the early stages of tumorigenesis, TGF-β signaling enforces profound tumor-suppressive effects, primarily by inducing cell cycle arrest, cellular senescence, autoph

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Kandagalla, Shivananda, Sharath Belenahalli Shekarappa, Gollapalli Pavan, Umme Hani та Manjunatha Hanumanthappa. "Exploring the Potential of Capsaicin Against Cancer Metastasis Based on TGF-β Signaling Modulation Through Module-based Network Pharmacology Approach". Current Drug Discovery Technologies 17, № 5 (2020): 647–60. http://dx.doi.org/10.2174/1570163816666190515104041.

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Background: Capsaicin is an active alkaloid /principal component of red pepper responsible for the pungency of chili pepper. Capsaicin by changing the intracellular redox homeostasis regulate a variety of signaling pathways ultimately producing a divergent cellular outcome. Several reports showed the potential of capsaicin against cancer metastasis, however unexplored molecular mechanism is still an active part of the research. Several growth factors have a critical role during cancer metastasis among them TGF- β signaling play a vital role. Methods: The present study aimed at analyzing capsai

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Drubay, Vincent, Nicolas Skrypek, Lucie Cordiez та ін. "TGF-βRII Knock-down in Pancreatic Cancer Cells Promotes Tumor Growth and Gemcitabine Resistance. Importance of STAT3 Phosphorylation on S727". Cancers 10, № 8 (2018): 254. http://dx.doi.org/10.3390/cancers10080254.

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Pancreatic adenocarcinoma (PDAC) is one of the most deadly cancers in the Western world because of a lack of early diagnostic markers and efficient therapeutics. At the time of diagnosis, more than 80% of patients have metastasis or locally advanced cancer and are therefore not eligible for surgical resection. Pancreatic cancer cells also harbour a high resistance to chemotherapeutic drugs such as gemcitabine that is one of the main palliative treatments for PDAC. Proteins involved in TGF-β signaling pathway (SMAD4 or TGF-βRII) are frequently mutated in PDAC (50–80%). TGF-β signalling pathway

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Działo, Edyta, Marcin Czepiel, Karolina Tkacz, Maciej Siedlar, Gabriela Kania та Przemysław Błyszczuk. "WNT/β-Catenin Signaling Promotes TGF-β-Mediated Activation of Human Cardiac Fibroblasts by Enhancing IL-11 Production". International Journal of Molecular Sciences 22, № 18 (2021): 10072. http://dx.doi.org/10.3390/ijms221810072.

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Cardiac fibrosis is a pathological process associated with the development of heart failure. TGF-β and WNT signaling have been implicated in pathogenesis of cardiac fibrosis, however, little is known about molecular cross-talk between these two pathways. The aim of this study was to examine the effect of exogenous canonical WNT3a and non-canonical WNT5a in TGF-β-activated human cardiac fibroblasts. We found that WNT3a and TGF-β induced a β-catenin-dependent response, whereas WNT5a prompted AP-1 activity. TGF-β triggered profibrotic signatures in cardiac fibroblasts, and co-stimulation with WNT

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Chow, Jimmy Y. C., Hui Dong, Khai T. Quach, Phuoc Nam Van Nguyen, Kevin Chen та John M. Carethers. "TGF-β mediates PTEN suppression and cell motility through calcium-dependent PKC-α activation in pancreatic cancer cells". American Journal of Physiology-Gastrointestinal and Liver Physiology 294, № 4 (2008): G899—G905. http://dx.doi.org/10.1152/ajpgi.00411.2007.

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Transforming growth factor-β (TGF-β) suppresses growth via the TGF-β-SMAD pathway but promotes growth in cancer cells with disrupted SMAD signaling and corresponds to an invasive phenotype. TGF-β also downregulates the tumor suppressor PTEN that is rarely mutated in sporadic pancreatic cancer; this downregulation may mediate cell proliferation and invasiveness, but the mechanism is unknown. Here, we examined whether TGF-β modulation of PTEN was mediated by protein kinase C (PKC). We have previously demonstrated that SMAD4-null BxPc-3 pancreatic cancer cells treated with TGF-β1 (10 ng/ml) suppr

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O'Connor, Kevin, Sofia Vidal-Cardenas, Haojian Zhang та ін. "Hyperactive Non-Canonical TGF-β Pathway Signaling in Fanconi Anemia Bone Marrow Stromal Cells Contributes to Growth Suppression". Blood 128, № 22 (2016): 1039. http://dx.doi.org/10.1182/blood.v128.22.1039.1039.

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Abstract Introduction: Fanconi anemia (FA) is the most common inherited bone marrow failure syndrome. FA patients develop bone marrow failure during the first decade of life due to attrition of hematopoietic stem cells (HSCs). FA is caused by autosomal recessive or X-linked mutations in one of nineteen FANC genes, the products of which cooperate in the FA/BRCA DNA repair pathway and regulate cellular resistance to genotoxic DNA cross-linking agents. Although its mechanism is unknown, bone marrow failure in FA may be the result, directly or indirectly, of hyperactivation of cell-autonomous or m

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