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2016 ; 9
(ä): 2131-41
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Downregulation of VEGFA inhibits proliferation, promotes apoptosis, and
suppresses migration and invasion of renal clear cell carcinoma
#MMPMID27110129
Zeng FC
; Zeng MQ
; Huang L
; Li YL
; Gao BM
; Chen JJ
; Xue RZ
; Tang ZY
Onco Targets Ther
2016[]; 9
(ä): 2131-41
PMID27110129
show ga
OBJECTIVE: The aim of this study was to investigate the effects of vascular
endothelial growth factor A (VEGFA) on cell proliferation, apoptosis, migration,
and invasion in renal clear cell carcinoma (RCCC). METHODS: Between June 2012 and
June 2015, RCCC tissues were obtained for the experimental group, and RCCC
adjacent tumor-free kidney parenchyma tissues were obtained for the control
group. VEGFA mRNA and protein expressions and phosphoinositide 3-kinase,
serine/threonine-specific protein kinase (AKT), and phosphorylated-AKT protein
expressions were detected. The chemically synthesized specific siRNA using RNA
interference technology was used to inhibit VEGFA gene expression in human RCCC
786-O cells. The negative control (NC) group was transfected with NC sequence,
and the blank group was transfected with no sequence. Flow cytometry, scratch
test, and cell-penetrating experiment were used to detect cell proliferation,
apoptosis, migration, and invasion of 786-O cells. RESULTS: Positive expression
of VEGFA protein was 60.62% in RCCC tissue and 18.34% in adjacent tissue with
statistically significant difference (P<0.001). VEGFA protein and mRNA
expressions were higher in RCCC tissue than those in adjacent tissue (both
P<0.01). VEGF expression in RCCC tissue was associated with Fuhrman grading and
American Joint Committee on Cancer staging (both P<0.05). After RCCC 786-O cells
transfecting the VEGFA siRNA, the VEGFA mRNA and protein expressions and
phosphoinositide 3-kinase and phosphorylated-AKT protein expressions were
significantly decreased, cell proliferation was remarkably inhibited, cell
apoptotic ratio was obviously increased, and migration distance and invasive cell
number were markedly decreased compared to those in the NC group and the blank
group (all P<0.05). CONCLUSION: Inhibition of VEGFA inhibited proliferation,
promoted apoptosis, and suppressed migration and invasion of RCCC 786-O cells.
VEGF has a potential role in diagnosis and therapy of RCCC.