COPB2 Is Upregulated in Prostate Cancer and Regulates PC-3 Cell Proliferation, Cell Cycle, and Apoptosis

Abstract

Background and aims: Transport of membranes and proteins in eukaryotic cells is mediated by vesicular carriers. Coatomer complex I (COPI)-coated vesicles are involved in the transport between endoplasmic reticulum (ER) and Golgi complex. Several studies indicated that some subunits of COPI were correlated with the cell proliferation of malignant tumors. The present study focused on the function of coatomer protein complex subunit β 2 (COPB2), one of seven proteins in COPI, in prostate cancer (PCa).

Methods: COPB2 gene expression was first analyzed by immunohistochemistry (IHC) in 15 paired PCa and carcinoma adjacent normal tissue from patients. To investigate the role of COPB2 in PCa, we used lentivirus-mediated small interfering RNA (siRNA) to knockdown COPB2 expression in human PCa cell line PC-3 and assessed it by RT-qPCR. Cellomics ArrayScan VTI imaging and colony formation were conducted to evaluate cell proliferation. Cell cycle phase arrest and apoptosis were assayed by flow cytometry.

Results: COPB2 gene was upregulated in the PCa tissue. Cell proliferation was significantly inhibited in COPB2-silenced PC-3 cells using both Cellomics ArrayScan VTI imaging and colony formation assays. S-phase cell counts were significantly decreased; G1- and G2-phase cell counts were significantly increased in COPB2-siRNA group than the control group. Apoptosis was significantly increased in COPB2-siRNA cells.

Conclusions: COPB2 significantly promoted PC-3 cell proliferation and colony formation through the cell cycle and apoptosis pathway. Moreover, COPB2 showed a clinical correlation and may serve as a biomarker for the detection for PCa.

Keywords: COPB2; Immunohistochemistry; Lentivirus; Proliferation; Prostate cancer.