MiR-302 a/b/c suppresses tumor angiogenesis in hepatocellular carcinoma by targeting MACC1

Y.-P. Cao, M. Pan, Y.-L. Song, H.-L. Zhang, H.-T. Sui, B.-C. Shan, H.-X. Piao

Department of Internal Medicine, Yanbian University, Yanji, Jilin, China. wmeqol@163.com

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• Oncology

OBJECTIVE: Hepatocellular carcinoma (HCC) is a hypervascularized tumor. Aberrant angiogenesis is the main cause, which results in cancer growth and progression. It has been showed that microRNA-302 cluster (miR-302) may be associated with angiogenesis. Here, we aimed to identify the role of miR-302a/b/c in the regulation of cell angiogenesis in HCC.
PATIENTS AND METHODS: MRNA expression of miR-302a/b/c and MACC1 was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The protein of MACC1 was measured using Western blot. Cells proliferation, migration, and invasion abilities were investigated via Cell Counting Kit-8 (CCK-8) assay or transwell assay, respectively. Tube formatting assays were used to explore the tube formation capacity. The interaction among miR-302a/b/c was analyzed by luciferase assay.
RESULTS: The expression of miR-302a/b/c was greatly reduced while MACC1 expression, whether mRNA or protein was conspicuously elevated in HCC tissues and cells. Then, functional experiment results showed miR-302a/b/c overexpression and MACC1 down-regulation inhibited the proliferation, migration, invasion ability, and tube formation capacity of HUVECs. In addition, we detected that miR-302a/b/c directly targeted MACC1 and suppressed MACC1 expression, and miR-302a/b/c could suppress tumor angiogenesis in HCC by targeting MACC1.
CONCLUSIONS: MiR-302a/b/c may function as a potential suppressor of tumor angiogenesis in HCC by targeting MACC1, indicating a promising target for HCC therapy.

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