CircPSMC3 inhibits cell proliferation and induces cell apoptosis in nasopharyngeal carcinoma by downregulating ROCK1

D.-Q. Guo, F. Liu, L. Zhang, N.-N. Bian, L.-Y. Liu, L.-X. Kong, Z.-G. Wang

Department of Otolaryngology Head and Neck Surgery, People’s Liberation Army Hospital 960 Ziboyuan District, Zibo, China. 1811592516@qq.com

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• Oncology

OBJECTIVE: Currently, the importance of circular RNAs in malignant tumors has attracted much attention. However, the role of circPSMC3 in nasopharyngeal carcinoma (NPC) remains unclear. The aim of this study was to investigate the function of circPSMC3 in the proliferation and apoptosis of NPC and to explore its possible underlying mechanism.

PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to determine the level of circPSMC3 in NPC tissues and cell lines. The association between circPSMC3 expression and patients’ prognosis was analyzed. CircPSMC3 lentivirus was constructed and transfected into NPC cells. Cell growth ability and apoptosis were detected through Cell Counting Kit-8 (CCK-8) assay, colony formation assay, and flow cytometry, respectively. Western blot was performed to analyze the target protein of circPSMC3. Furthermore, the function of circPSMC3 was explored in nude mice.

RESULTS: CircPSMC3 was lowly expressed in NPC tissues compared with adjacent normal tissues. Low circPSMC3 expression was associated with poor prognosis of NPC patients. Meanwhile, the expression of circPSMC3 was significantly down-regulated in NPC cell lines as well. The growth ability of NPC cells was markedly inhibited after circPSMC3 was overexpressed. Overexpression of circPSMC3 significantly promoted the apoptosis of NPC cells in vitro. ROCK1 expression decreased markedly via overexpression of circPSMC3. Furthermore, tumor formation was inhibited after the up-regulation of circPSMC3 in vivo.

CONCLUSIONS: CircPSMC3 could suppress cell growth and promote cell apoptosis in NPC by downregulating ROCK1.

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