Downregulation of COPB2 by RNAi inhibits growth of human cholangiocellular carcinoma cells

Z.-S. Li, C.-H. Liu, Z. Liu, C.-L. Zhu, Q. Huang

Department of General Surgery, the Affiliated Provincial Hospital of Anhui Medical University, Hefei, Anhui, China. huangqiangjiaoshou@163.com

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• Oncology

OBJECTIVE: The present study aimed to explore the contribution of COPB2 (coatomer subunit beta) towards the tumorigenesis of cholangiocellular carcinomas and to elucidate the underlying mechanism(s).

MATERIALS AND METHODS: Expression of COPB2 mRNA by RBE and QBC939 cholangiocellular carcinoma cell lines was determined by qRT-PCR. We, then, silenced COPB2 expression in RBE cells by infection with a COPB2-siRNA lentivirus and measured the proliferation, cell-cycle distribution, and apoptosis of transduced cells.

RESULTS: COPB2 was highly expressed in RBE and QBC939 cholangiocellular carcinoma cell lines. Infection with COPB2-siRNA lentivirus in RBE cells significantly decreased COPB2 expression. More so, silencing of COPB2 by COPB2-siRNA significantly suppressed the proliferation and promoted the apoptosis of RBE cells by arresting transduced cells in the G1 phase.

CONCLUSIONS: Our results demonstrate that the COPB2 gene is highly expressed in cholangiocellular carcinoma cell lines, wherein knockdown inhibited the proliferation and promoted the arrest of cell-cycle progression and the apoptosis of cholangiocellular carcinomas. COPB2 may constitute an attractive target for therapeutic strategies against cholangiocellular cancers.

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