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2018 ; 18
(ä): 83
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MiR-218 regulates epithelial-mesenchymal transition and angiogenesis in
colorectal cancer via targeting CTGF
#MMPMID29977158
Lun W
; Wu X
; Deng Q
; Zhi F
Cancer Cell Int
2018[]; 18
(ä): 83
PMID29977158
show ga
BACKGROUND: Endothelial-to-mesenchymal transition (EMT) and angiogenesis play
important roles in colorectal cancer (CRC) development. Connective tissue growth
factor (CTGF) has been reported to promote several kinds of cancer progression
and miR-218 has been identified as a tumor suppressor miRNA. However, little is
known about the function of miR-218 in CRC. Here we investigated the effects of
miR-218 on EMT and angiogenesis process in CRC cells. As well, the relation
between miR-218 and CTGF was identified. The mechanism of miR-218's function was
illustrated. METHODS: CRC cell lines were transfected with miR-218 mimics.
Proliferation, migration and angiogenesis were identified by MTT assay, Transwell
assay, colony formation assay and tube formation assay. Protein and mRNA
expression levels of associated genes were measured by Western blotting and
RT-PCR. Dual luciferase assay was used to determine the relation of miR-218 and
CTGF. RESULTS: miR-218 was down-regulated in CRC cell lines and over expression
of miR-218 could significantly inhibit EMT and angiogenesis. CTGF was a direct
target of miR-218. Up regulation of CTGF level after miR-218 transfection could
sufficiently rescue the suppression effects on EMT and angiogenesis. CONCLUSION:
miR-218 directly targets CTGF and inhibits its expression, leading to suppression
on EMT and angiogenesis of CRC cells. miR-218 might be used as potential
therapeutic strategy for CRC treatment.