Roles of microRNA‑186 and vascular endothelial growth factor in hepatocellular carcinoma complicated with portal vein tumor thrombus
Affiliations: Department of Hepatobiliary Surgery, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China, The Second Ward of General Surgery Department, Ankang City Central Hospital, Ankang, Shaanxi 725000, P.R. China
- Published online on: August 3, 2020 https://doi.org/10.3892/etm.2020.9092
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The present study aims to investigate the role and underlying mechanism of microRNA (miR)‑186 in patients with hepatocellular carcinoma (HCC) complicated with portal vein tumor thrombus. Blood samples from 29 HCC patients with portal vein tumor thrombus were collected between January 2014 and September 2015 in Huai'an First People's Hospital, while blood from 36 HCC patients without vein tumor thrombus was also collected in the same period. In addition, tumor thrombus specimens were collected from the HCC patients with portal vein tumor thrombus, and peritumoral tissues of the tumor thrombus were used as the control. Reverse transcription‑quantitative polymerase chain reaction, ELISA and western blot analyses were applied to detect vascular endothelial growth factor (VEGF) expression at the mRNA and protein levels. Bioinformatics prediction was used to predict the target of miR‑186, and then miR‑186 expression was detected. Furthermore, dual‑luciferase reporter assay was used to validate whether miR‑186 directly targeted VEGF. Following transfection with agomiR‑186, the expression levels of miR‑186 and VEGF were detected, while MTT assay was used to detect EA.hy926 cell proliferation subsequent to small interfering RNA (siRNA) silencing. The results identified that VEGF was significantly increased in the tumor thrombus and blood samples of HCC patients with vein tumor thrombus at the mRNA and protein levels, while miR‑186 expression was significantly decreased (P<0.05). Following silencing VEGF by siRNA transfection, the proliferation of EA.hy926 cells was inhibited. In addition, VEGF expression was significantly decreased and cell proliferation was reduced when upregulating miR‑186. Dual‑luciferase reporter assay demonstrated that miR‑186 regulated VEGF expression through complementary binding to 3'‑untranslated region. In conclusion, VEGF was significantly increased in tumor thrombus and blood samples from HCC patients with vein tumor thrombus, which may be associated with the downregulation of miR‑186. Thus, miR‑186 may promote the development and progression of vein tumor thrombus in HCC.