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MIR‐27a regulates the TGF‐β signaling pathway by targeting SMAD2 and SMAD4 in lung cancer
Author(s) -
Chae DongKyu,
Ban Eunmi,
Yoo Young Sook,
Kim Eunice EunKyeong,
Baik JaHyun,
Song Eun Joo
Publication year - 2017
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.22655
Subject(s) - biology , carcinogenesis , cancer research , oncogene , downregulation and upregulation , transforming growth factor , signal transduction , cancer , lung cancer , acvrl1 , cell cycle , suppressor , cell growth , microrna , gene , microbiology and biotechnology , endoglin , genetics , medicine , stem cell , cd34
The transforming growth factor‐β (TGF‐β) signaling pathway is associated with carcinogenesis and various biological processes. SMAD2 and SMAD4 , which are putative tumor suppressors, have an important role in TGF‐β signaling. The aberrant expression of these genes is implicated in some cancers. However, the mechanisms of SMAD2 and SMAD4 dysregulation are poorly understood. In this study, we observed that miR‐27a was upregulated in lung cancer cell lines and patients. In addition, SMAD2 and SMAD4 genes were identified as targets of miR‐27a by several target prediction databases and experimental validation. Functional studies revealed that miR‐27a overexpression decreased SMAD2 and SMAD4 mRNA and protein levels. Furthermore, miR‐27a contributed to cell proliferation and invasion by inhibiting TGF‐β‐induced cell cycle arrest. These results suggest that miR‐27a may function as an oncogene by regulating SMAD2 and SMAD4 in lung cancer. Thus, miR‐27a may be a potential target for cancer therapy.