Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28030804
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Tumor-suppressive microRNA-218 inhibits tumor angiogenesis via targeting the mTOR
component RICTOR in prostate cancer
#MMPMID28030804
Guan B
; Wu K
; Zeng J
; Xu S
; Mu L
; Gao Y
; Wang K
; Ma Z
; Tian J
; Shi Q
; Guo P
; Wang X
; He D
; Du Y
Oncotarget
2017[Jan]; 8
(5
): 8162-8172
PMID28030804
show ga
MicroRNAs, a kind of small non-coding RNAs, can regulate gene expression by
targeting mRNAs for translational repression or degradation. Much evidence has
suggested that miR-218 was a tumor suppressor in many human cancers including
prostate cancer. However, the underlying role of miR-218 in tumor angiogenesis
and the mechanisms in PCa and other cancers remains to be unclear. Here in this
present study, we demonstrated that miR-218 inhibited the tumor angiogenesis of
PCa cells in vitro and in vivo. RICTOR, the mTOR component 2, was a direct target
of miR-218 and miR218-RICTOR-VEGFA axis was the mechanism inhibiting the tumor
angiogenesis of PCa cells. RICTOR knockdown phenocopied miR-218 overexpression in
inhibiting prostate cancer angiogenesis. Altogether, our findings indicate that
down-regulation of miR-218 contributes to tumor angiogenesis through RICTOR/VEGFA
axis in PCa, providing new insights into the potential mechanisms of PCa
oncogenesis and revealing the potential of miR-218 as a useful serum biomarker
and a new therapeutic target for human PCa.
free
free
free
