ArticleFrontiers in physiology2011
Regulation of TGF-β1-Induced Pro-Apoptotic Signaling by Growth Factor Receptors and Extracellular Matrix Receptor Integrins in the Liver.
Article in Frontiers in physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
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- Targeting Oxidative Stress: The Potential of Vitamin C in Protecting against Liver Damage after Electron Beam Therapy.Biomedicines · 2024Article
- Hepatic Extracellular Matrix and Its Role in the Regulation of Liver Phenotype.Seminars in liver disease · 2024Review
- Human induced pluripotent stem cell-derived closed-loop cardiac tissue for drug assessment.iScience · 2024Article
- Unusual effects of a nanoporous gold substrate on cell adhesion and differentiation because of independent multi-branch signaling of focal adhesions.Journal of materials science. Materials in medicine · 2023Article
- SEMA7AR148W mutation promotes lipid accumulation and NAFLD progression via increased localization on the hepatocyte surface.JCI insight · 2022Article
- Review
- Clinically Translatable Approaches of Inhibiting TGF-β to Target Cancer Stem Cells in TNBC.Biomedicines · 2021Review
- EMP2 induces cytostasis and apoptosis via the TGFβ/SMAD/SP1 axis and recruitment of P2RX7 in urinary bladder urothelial carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Integrin alpha-v/beta3 expression in equine lungs and jejunum.Canadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2020Article
- Klotho and the Treatment of Human Malignancies.Cancers · 2020Review
- The Matrisome, Inflammation, and Liver Disease.Seminars in liver disease · 2020Review
- A Perspective on the Development of TGF-β Inhibitors for Cancer Treatment.Biomolecules · 2019Review
- Review
- Validation of Hepatocellular Carcinoma Experimental Models for TGF-β Promoting Tumor Progression.Cancers · 2019Review
- ITGA5 inhibition in pancreatic stellate cells attenuates desmoplasia and potentiates efficacy of chemotherapy in pancreatic cancer.Science advances · 2019Article
- TGF-β-Mediated Epithelial-Mesenchymal Transition and Cancer Metastasis.International journal of molecular sciences · 2019Review
- Pro-atherogenic proteoglycanase ADAMTS-1 is down-regulated by lauric acid through PI3K and JNK signaling pathways in THP-1 derived macrophages.Molecular biology reports · 2019Article
- Regulation of interferon signaling and HCV‑RNA replication by extracellular matrix.International journal of molecular medicine · 2018Article
- Intracellular IL-37b interacts with Smad3 to suppress multiple signaling pathways and the metastatic phenotype of tumor cells.Oncogene · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) often arises from chronically diseased livers. Persistent liver inflammation causes the accumulation of excessive extracellular matrix (ECM) proteins and impairs the liver function, finally leading to the development of HCC. A pleiotropic cytokine, transforming growth factor (TGF)-β1, plays critical roles throughout the process of fibrogenesis and hepatocarcinogenesis. In the liver, TGF-β1 inhibits the proliferation of hepatocytes and stimulates the production of ECM from hepatic stellate cells (HSCs) to maintain tissue homeostasis. During disease progression, both growth factors/cytokines and the ECM alter the TGF-β1 signals by modifying the phosphorylation of Smad proteins at their C-terminal and linker regions. TGF-β1 stimulates the expression of integrins, cellular receptors for ECM, along with an increase in ECM accumulation. The activation of integrins by the ECM modulates the response to TGF-β1 in hepatic cells, resulting in their resistance to TGF-β1-induced growth suppression in hepatocytes and the sustained production of ECM proteins in activated HSCs/myofibroblasts. Both growth factor receptors and integrins modify the expression and/or functions of the downstream effectors of TGF-β1, resulting in the escape of hepatocytes from TGF-β1-induced apoptosis. Recent studies have revealed that the alterations of Smad phosphorylation that occur as the results of the crosstalk between TGF-β1, growth factors and integrins could change the nature of TGF-β1 signals from tumor suppression to promotion. Therefore, the modification of Smad phosphorylation could be an attractive target for the prevention and/or treatment of HCC.
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