ArticleOncogene2002
Downregulation of Betaig-h3 gene is causally linked to tumorigenic phenotype in asbestos treated immortalized human bronchial epithelial cells.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 58 citations in OpenAlex.
- Soluble TGFBI aggravates the malignancy of cholangiocarcinoma through activation of the ITGB1 dependent PPARγ signalling pathway.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Bigh3 silencing increases retinoblastoma tumor growth in the murine SV40-TAg-Rb model.Oncotarget · 2017Article
- Knockdown of cullin 4A inhibits growth and increases chemosensitivity in lung cancer cells.Journal of cellular and molecular medicine · 2016Article
- The role of TGFBI (βig-H3) in gastrointestinal tract tumorigenesis.Molecular cancer · 2015Article
- TGFBI expression is an independent predictor of survival in adjuvant-treated lung squamous cell carcinoma patients.British journal of cancer · 2014Article
- The role of novel and known extracellular matrix and adhesion molecules in the homeostatic and regenerative bone marrow microenvironment.Cell adhesion & migration · 2014Review
- Study designs to investigate Nox1 acceleration of neoplastic progression in immortalized human epithelial cells by selection of differentiation resistant cells.Redox biology · 2014Review
- The insoluble TGFBIp fraction of the cornea is covalently linked via a disulfide bond to type XII collagen.Biochemistry · 2013Article
- Article
- Matrix metalloproteinase 9 (MMP-9)-dependent processing of βig-h3 protein regulates cell migration, invasion, and adhesion.The Journal of biological chemistry · 2012Article
- The role of TGFBI in mesothelioma and breast cancer: association with tumor suppression.BMC cancer · 2012Article
- TGFBI promoter hypermethylation correlating with paclitaxel chemoresistance in ovarian cancer.Journal of experimental & clinical cancer research : CR · 2012Article
- Transforming growth Factor-Beta-Induced Protein (TGFBI)/(βig-H3): a matrix protein with dual functions in ovarian cancer.International journal of molecular sciences · 2012Review
- Transforming growth factor-β-induced protein (TGFBI) suppresses mesothelioma progression through the Akt/mTOR pathway.International journal of oncology · 2011Article
- TGFBI expression reduces in vitro and in vivo metastatic potential of lung and breast tumor cells.Cancer letters · 2011Article
- MiR-21 plays an important role in radiation induced carcinogenesis in BALB/c mice by directly targeting the tumor suppressor gene Big-h3.International journal of biological sciences · 2011Article
- TGFBI expression is associated with a better response to chemotherapy in NSCLC.Molecular cancer · 2010Article
- Expression analysis of human pterygium shows a predominance of conjunctival and limbal markers and genes associated with cell migration.Molecular vision · 2009Article
- TGFBI deficiency predisposes mice to spontaneous tumor development.Cancer research · 2009Article
- Methylation screening of the TGFBI promoter in human lung and prostate cancer by methylation-specific PCR.BMC cancer · 2008Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although Betaig-h3 gene has been suggested to modulate cell adhesion and tumor formation, its physiological functions are not well understood. Using human papillomavirus immortalized human bronchial epithelial (BEP2D) cells, we found that Betaig-h3 expression was markedly decreased in asbestos-induced tumorigenic cells. Fusion of tumorigenic and control BEP2D cells resulted in the recovery of Betaig-h3 gene expression to control level and the loss of tumorigenic phenotype. Furthermore, ectopic expression of Betaig-h3 gene in asbestos-induced tumorigenic cells inhibited cell growth in vitro, anchorage independent phenotype, as well as tumorigenicity in nude mice. Betaig-h3 gene is ubiquitously expressed in various normal human tissues, with the exception of the brain, where there is little or no expression. In contrast, there was a decrease or absence in expression of the Betaig-h3 gene in 14 human tumor cell lines of diverse histological types examined, when compared with normal human cells or tissues. The result strongly suggests that loss of Betaig-h3 expression is a frequent event in human cancer and causally related to acquisition of tumorigenic phenotype in asbestos-treated BEP2D cells.
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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.