RRC ID 52485
著者 Goto M, Osada S, Imagawa M, Nishizuka M.
タイトル FAD104, a regulator of adipogenesis, is a novel suppressor of TGF-β-mediated EMT in cervical cancer cells.
ジャーナル Sci Rep
Abstract Epithelial-to-mesenchymal transition (EMT) is a biological process in which epithelial cells translate into a mesenchymal phenotype with invasive capacities, contributing to tumour progression, metastasis, and the acquisition of chemotherapy resistance. To identify new therapeutic targets for cancers, it is important to clarify the molecular mechanism of induction of EMT. We have previously reported that fad104, a positive regulator of adipocyte differentiation, suppressed the invasion and metastasis of melanoma and breast cancer cells. In this study, we showed that FAD104 functions as a novel suppressor of transforming growth factor-β (TGF-β)-mediated EMT in cervical cancer cells. Expression of FAD104 is upregulated during TGF-β-mediated EMT in human cervical cancer HeLa cells. Reduction of fad104 expression enhanced TGF-β-mediated EMT and migration in HeLa cells. Conversely, overexpression of FAD104 suppressed TGF-β-induced EMT. In addition, we showed that FAD104 negatively regulated phosphorylation of Smad2 and Smad3 but positively regulated phosphorylation of Smad1/5/8 via treatment with TGF-β. These findings demonstrate that FAD104 is a novel suppressor of TGF-β signalling and represses TGF-β-mediated EMT in cervical cancer cells.
巻・号 7(1)
ページ 16365
公開日 2017-11-27
DOI 10.1038/s41598-017-16555-3
PII 10.1038/s41598-017-16555-3
PMID 29180690
PMC PMC5703855
MeSH Adipogenesis* / genetics Biomarkers Cell Line, Tumor Epithelial-Mesenchymal Transition* / genetics Female Fibronectins / genetics Fibronectins / metabolism* Gene Expression Gene Knockdown Techniques HeLa Cells Humans Signal Transduction Smad Proteins / metabolism Transforming Growth Factor beta / metabolism* Uterine Cervical Neoplasms / genetics Uterine Cervical Neoplasms / metabolism*
IF 3.998
引用数 6
リソース情報
ヒト・動物細胞 HeLa(RCB0007)