ArticleInternational journal of oncology2011
Transforming growth factor-β-induced protein (TGFBI) suppresses mesothelioma progression through the Akt/mTOR pathway.
Article in International journal of oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- Exploring mechanisms of scar-free skin wound healing in adult zebrafish in comparison to mouse.PLoS genetics · 2026Article
- Integrative Transcriptomic and Proteomic Analysis RevealsAnimals : an open access journal from MDPI · 2025Article
- Intrinsic PDL1 Signaling Modulates TGFBI-Mediated Growth Suppression in Lung Adenocarcinoma.Cancer science · 2025Article
- A bibliometric analysis of malignant pleural mesothelioma from 2010 to 2023.Journal of thoracic disease · 2025Article
- mTORC1 regulates the proliferation of SOX9Histochemistry and cell biology · 2025Article
- Hypoxic conditions affect transcriptome of endometrial stromal cells in endometriosis and promote TGFBI axis.Frontiers in endocrinology · 2024Article
- Niclosamide Suppresses Migration and Invasion of Human Osteosarcoma Cells by Repressing TGFBI Expression via the ERK Signaling Pathway.International journal of molecular sciences · 2022Article
- Pan-Cancer Analysis of the Associations of TGFBI Expression With Prognosis and Immune Characteristics.Frontiers in molecular biosciences · 2021Article
- Molecular mechanism of microRNA-21 promoting Schwann cell proliferation and axon regeneration during injured nerve repair.RNA biology · 2020Article
- Epigenetic silencing of TGFBI confers resistance to trastuzumab in human breast cancer.Breast cancer research : BCR · 2019Article
- TGFBI Promotes Tumor Growth and is Associated with Poor Prognosis in Oral Squamous Cell Carcinoma.Journal of Cancer · 2019Article
- TGFBI Expressed by Bone Marrow Niche Cells and Hematopoietic Stem and Progenitor Cells Regulates Hematopoiesis.Stem cells and development · 2018Article
- Dysregulation of the MiR-449b target TGFBI alters the TGFβ pathway to induce cisplatin resistance in nasopharyngeal carcinoma.Oncogenesis · 2018Article
- Bigh3 silencing increases retinoblastoma tumor growth in the murine SV40-TAg-Rb model.Oncotarget · 2017Article
- Consensus Report of the 2015 Weinman International Conference on Mesothelioma.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2016Article
- The role of cancer-associated fibroblasts in esophageal cancer.Journal of translational medicine · 2016Review
- The role of TGFBI (βig-H3) in gastrointestinal tract tumorigenesis.Molecular cancer · 2015Article
- MicroRNA-21 Regulates PI3K/Akt/mTOR Signaling by Targeting TGFβI during Skeletal Muscle Development in Pigs.PloS one · 2015Article
- Gallotannin imposes S phase arrest in breast cancer cells and suppresses the growth of triple-negative tumors in vivo.PloS one · 2014Article
- Discoidin domain receptor 1 contributes to tumorigenesis through modulation of TGFBI expression.PloS one · 2014Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
As an uncommon cancer, mesothelioma is very hard to treat with a low average survival rate owing to its usual late detection and being highly invasive. The link between asbestos exposure and the development of mesothelioma in humans is unequivocal. TGFBI, a secreted protein that is induced by transforming growth factor-β in various human cell types, has been shown to be associated with tumorigenesis in various types of tumors. It has been demonstrated that TGFBI expression is markedly suppressed in asbestos-induced tumorigenic cells, while an ectopic expression of TGFBI significantly suppresses tumorigenicity and progression in human bronchial epithelial cells. In order to delineate a potential role of TGFBI in mediating the molecular events that occur in mesothelioma tumorigenesis, we generated stable TGFBI knockdown mutants from the mesothelium cell line Met-5A by using an shRNA approach, and secondly created ectopic TGFBI overexpression mutants from the mesothelioma cell line H28 in which TGFBI is absent. We observed that in the absence of TGFBI, the knockdown mesothelial and mesothelioma cell lines exhibited an elevated proliferation rate, enhanced plating efficiency, increased anchorage-independent growth, as well as an increased cellular protein synthesis rate as compared with their respective controls. Furthermore, cell cycle regulatory proteins c-myc/cyclin D1/phosphor-Rb were upregulated; a more active PI3K/Akt/mTOR signaling pathway was also detected in TGFBI-depleted cell lines. These findings suggest that TGFBI may repress mesothelioma tumorigenesis and progression via the PI3K/Akt signaling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.