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2018 ; 18
(ä): 105
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miR-145 and miR-497 suppress TGF-?-induced epithelial-mesenchymal transition of
non-small cell lung cancer by targeting MTDH
#MMPMID30065618
Yin Q
; Han Y
; Zhu D
; Li Z
; Shan S
; Jin W
; Lu Q
; Ren T
Cancer Cell Int
2018[]; 18
(ä): 105
PMID30065618
show ga
BACKGROUND: MicroRNAs (miRNAs) have been reported to play crucial roles in
multiple cancers including non-small cell lung cancer (NSCLC). Here, we
investigated the role of miR-145 and miR-497 in TGF-?-induced
epithelial-mesenchymal transition (EMT) process of NSCLC. METHODS: We performed
quantitative real time PCR (qRT-PCR) to detect the expression level of miR-145
and miR-497 in NSCLC cell lines. Then in the presence/absence of TGF-?, we
transfected miRNA mimics or inhibitor into A549 and H1299 cells and investigated
the role of miR-145 and miR-497 in cell migration and invasion using transwell
and wound-healing assay. The regulation role of miR-145 and miR-497 on Metadherin
(MTDH) was determined by luciferase assay. The expression level of MTDH and EMT
markers E-cadherin and vimentin were detected on mRNA and protein level. RESULTS:
In our study, our results showed that miR-145 and miR-497 were downregulated in
NSCLC cell lines. Overexpression of miR-145 and miR-497 inhibited TGF-?-induced
EMT and suppressed cancer cell migration and invasion, while the opposite results
were observed in cells transfected with miR-145 or miR-497 inhibitor. Moreover,
the luciferase assay confirmed that miR-145 and miR-497 attenuated MTDH
expression by directly binding 3'-UTR of MTDH mRNA and exert the
tumor-suppression role. CONCLUSIONS: Overall, we demonstrated that miR-145 and
miR-497 functioned as EMT-suppressor in NSCLC by targeting MTDH, provided new
evidence that miR-145 and miR-497 as potential therapeutic targets.
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