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2017 ; 13
(5
): 3247-3252
Nephropedia Template TP
gab.com Text
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English Wikipedia
MicroRNA-320a is downregulated in non-small cell lung cancer and suppresses tumor
cell growth and invasion by directly targeting insulin-like growth factor 1
receptor
#MMPMID28521431
Wang J
; Shi C
; Wang J
; Cao L
; Zhong L
; Wang D
Oncol Lett
2017[May]; 13
(5
): 3247-3252
PMID28521431
show ga
Accumulating evidence has demonstrated that microRNAs (miRs/miRNAs) are
implicated in carcinogenesis and cancer progression, and can function as
oncogenes or tumor suppressor genes in human cancer types. Previous profile
studies of miRNA expression levels have revealed that miR-320a was downregulated
in breast cancer, colon cancer, bladder cancer, glioblastoma and salivary adenoid
cystic carcinoma. However, its expression level, potential functions and the
mechanisms underlying its functions in non-small cell lung cancer (NSCLC) require
further investigation. The present study investigated the expression level,
biological roles and underlying molecular mechanisms of miR-320a in NSCLC. The
expression levels of miR-320a in NSCLC tissue and cell lines were detected using
the reverse transcription-quantitative polymerase chain reaction. Cell
proliferation and Transwell invasion assays were performed to examine the effects
of miR-320a on NSCLC cells. In addition, bioinformatic analysis, western blot
analysis and luciferase reporter assays were performed to identify the direct
gene target of miR-320a in NSCLC. In the present study it was demonstrated that
miR-320a was significantly downregulated in NSCLC tissues and cell lines. Ectopic
overexpression of miR-320a suppressed the proliferation and invasion of NSCLC
cells. Further studies indicated that miR-320a directly targeted the
3'-untranslated region of insulin-like growth factor 1 receptor (IGF-1R) and
suppressed its expression at the mRNA and protein levels. As well as restoring
the miR-320a expression level, the knockdown of IGF-1R also decreased the growth
and invasion of the NSCLC cells. These results suggested that miR-320a served as
a tumor suppressor in the NSCLC cells by directly targeting IGF-1R. Therefore,
miR-320a should be investigated as a therapeutic target for the treatment of
NSCLC.