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2016 ; 7
(48
): 79805-79813
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
MicroRNA-206 attenuates the growth and angiogenesis in non-small cell lung cancer
cells by blocking the 14-3-3?/STAT3/HIF-1?/VEGF signaling
#MMPMID27806334
Xue D
; Yang Y
; Liu Y
; Wang P
; Dai Y
; Liu Q
; Chen L
; Shen J
; Ju H
; Li Y
; Tan Z
Oncotarget
2016[Nov]; 7
(48
): 79805-79813
PMID27806334
show ga
Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related
mortality worldwide. Angiogenesis is the major hallmark in NSCLC. So, further
elucidation of molecular mechanisms underlying the angiogenesis of NSCLC is
urgently needed. Here, we found that microRNA-206 (miR-206) decreased the
angiogenic ability in NSCLC via inhibiting the 14-3-3?/STAT3/HIF-1?/VEGF pathway.
Briefly, 14-3-3? bond with phosphorylated-STAT3, and in turn, elevated the
expression of HIF-1?. Then, by enhancing the recruitment of HIF-1? to VEGF
promoter, 14-3-3? increased the angiogenesis. However, miR-206 decreased the
angiogenesis by targeting 14-3-3?, and inhibiting the STAT3/HIF-1?/VEGF pathway.
In NSCLC cell xenograft model, either overexpression of miR-206 or inhibition of
14-3-3? inhibited the STAT3/HIF-1?/VEGF pathway and decreased the tumor growth
and angiogenesis. Furthermore, there was a negative correlation between miR-206
and 14-3-3? in NSCLC specimens. NSCLC patients with low expressions of miR-206
but high expressions of 14-3-3? had the worst survival. Collectively, our
findings provided the underlying mechanisms of miR-206/14-3-3? in tumor growth
and angiogenesis, and implicated miR-206 and 14-3-3? as potential therapeutic
targets for NSCLC.