Effects of VEGF/VEGFR/K-ras signaling pathways on miRNA21 levels in hepatocellular carcinoma tissues in rats.
The aim of this study was to investigate the effects of the vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR)/K-ras signaling pathways on miRNA21 levels in hepatocellular carcinoma tissues in rats. Eighteen male Sprague-Dawley rats were randomly divided into normal control, model, and VEGF blocking agent groups (N = 6/group). The expression of VEGF mRNA, K-ras protein, and miRNA21 increased significantly (P < 0.05) in the model group compared with the normal control group, and decreased dramatically in the VEGF blocking agent group compared to the model group. The expression of VEGFR mRNA in the model group was higher than that of the control group, and the expression of VEGFR mRNA in the VEGF blocking agent group was significantly higher than that of the control group (P < 0.05). Statistically, there was no difference between the expression of VEGFR mRNA for the VEGF blocking agent group and the model group (P > 0.05). Finally, the expression of the miRNA21 gene in the VEGF blocking agent group was higher than in the control group, and there was a significant statistical difference noted; Pearson's correlation analysis demonstrated that the expression of K-ras protein was positively correlated with miRNA21 in the experimental groups (P = 0.001). The above results showed that the VEGF/VEGFR/K-ras signaling pathway might promote the occurrence and development of hepatocellular carcinoma cells through regulating expression of miRNA21, which has potential clinical value for the development of therapies against biological targets and determining prognosis for patients with hepatocellular carcinoma.
Medical College, Xinxiang Medical University, Xinxiang, Henan Province, China.
J Z
JZ
Gao
Medical College, Xinxiang Medical University, Xinxiang, Henan Province, China.
Y L
YL
Wang
Department of Pathology, General Hospital of the People's Liberation Army, Beijing, China.
J
J
Li
Department of Pathology, General Hospital of the People's Liberation Army, Beijing, China weilx301@263.net.
L X
LX
Wei
D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000139:chemically induced / Q000235:genetics* / Q000473:pathology; D004052:Diethylnitrosamine / Q000633:toxicity; D004195:Disease Models, Animal; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008113:Liver Neoplasms / Q000139:chemically induced / Q000235:genetics* / Q000473:pathology; D035683:MicroRNAs / Q000096:biosynthesis* / Q000235:genetics; D009389:Neovascularization, Pathologic / Q000235:genetics / Q000473:pathology; D016283:Proto-Oncogene Proteins p21(ras) / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000235:genetics; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000235:genetics; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000096:biosynthesis* / Q000235:genetics
C528430:Kras protein, rat; C524940:MIRN21 microRNA, human; D035683:MicroRNAs; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D004052:Diethylnitrosamine; C501162:FLT1 protein, human; C000602029:Kdr protein, rat; D040281:Vascular Endothelial Growth Factor Receptor-1; D040301:Vascular Endothelial Growth Factor Receptor-2; D016283:Proto-Oncogene Proteins p21(ras)