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2015 ; 8
(ä): 2689-97
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miR-98 targets ITGB3 to inhibit proliferation, migration, and invasion of
non-small-cell lung cancer
#MMPMID26445551
Ni R
; Huang Y
; Wang J
Onco Targets Ther
2015[]; 8
(ä): 2689-97
PMID26445551
show ga
BACKGROUND: Accumulating evidence has emphasized causative links between aberrant
microRNA (miR) expression patterns and cancer development. Abnormally expressed
miRNA-98 (miR-98) was found in certain types of human cancers. The biological
roles of miR-98 in lung cancer, however, remain largely undefined. METHODS: We
evaluated the expression of miR-98 in normal lung tissues, lung cancer tissues,
normal human bronchial epithelial cells, and lung cancer cells using quantitative
real-time polymerase chain reaction. Effect of miR-98 on proliferation of lung
cancer cells was investigated using MTT assay and colony formation assay.
Transwell assay was used to assess the effects of miR-98 on migration and
invasion of lung cancer cells. Whether miR-98 targets the 3'-untranslated region
(3'-UTR) of integrin ?3 (ITGB3) coding gene ITGB3 mRNA was ascertained using
luciferase reporter assay. Finally, we transplanted miR-98 expressing A549 cells
into nude mice to observe the effect of miR-98 on tumor growth in vivo. RESULTS:
We confirmed that miR-98 was frequently low expressed in lung cancer tissues and
human lung cancer cells. Reintroduction of miR-98 into lung cancer cells
inhibited cell proliferation, migration, and invasion in vitro and suppressed
tumor formation in a nude mouse model. Furthermore, we identified that miR-98
exerted inhibitory roles by directly binding to 3'-UTR of ITGB3 mRNA, thus
negatively regulated the expression of ITGB3. Interestingly, upon restoring the
expression of ITGB3, the effect of miR-98 on cell proliferation was partially
reversed. CONCLUSION: Our findings suggest that miR-98 prevents proliferation,
migration, and invasion of lung cancer cells by directly binding to the 3'-UTR of
ITGB3 mRNA and could be a promising treatment option in anticancer therapy.