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2016 ; 9
(ä): 1489-98
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miR-32 inhibits proliferation, epithelial-mesenchymal transition, and metastasis
by targeting TWIST1 in non-small-cell lung cancer cells
#MMPMID27042117
Li L
; Wu D
Onco Targets Ther
2016[]; 9
(ä): 1489-98
PMID27042117
show ga
BACKGROUND: By analyzing published microRNA microarray studies, miR-32 was found
to be markedly reduced in non-small-cell lung cancer (NSCLC) tissues compared
with that in nontumor tissues. However, little is known about its role and
molecular mechanism involved in NSCLC development and progression. Here, we
report the effect of miR-32 on NSCLC cell proliferation, epithelial-mesenchymal
transition (EMT), and metastasis. METHODS: Quantitative real-time PCR was
performed to detect the expression level of miR-32 in primary NSCLC cases and
cell lines. miR-32-overexpressing H1299 and A549 cells were constructed by
lipofection transfection. MTT, transwell chamber, and Western blot assays were
used to assess the effect of miR-32 on proliferation, EMT, and metastasis of
NSCLC cells, respectively. Target prediction and luciferase reporter assays were
performed to investigate the targets of miR-32. Tumor formation assay in vivo was
performed to investigate the antitumor effect of miR-32. RESULTS: An inverse
correlation existed between miR-32 expression level and NSCLC cell proliferation,
EMT, and metastasis, and upregulation of miR-32 repressed NSCLC cell
proliferation, EMT, and metastasis. Moreover, we identified and validated that
TWIST1 was a direct target of miR-32, and miR-32 regulated NSCLC cell
proliferation, EMT, and metastasis, at least in part via modulation of TWIST1.
The animal experiments showed that overexpression of miR-32 inhibited the growth
of NSCLC tumors in vivo.