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CircZNF652 accelerates the proliferation and migration of primary lung carcinoma cells by downregulating miR-766
Abstract
Purpose: To explore the biological functions and molecular mechanism of circZNF652 involvement in primary lung carcinoma.
Methods: CircZNF652 levels in primary lung carcinoma cases and controls were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Its prognostic value in primary lung carcinoma was examined by depicting it with Kaplan-Meier curves. The biological functions of circZNF652 in regulating proliferative and migratory capacities in A549 and SPC-A-1 cells were analyzed from the curves. Interaction between circZNF652 and its downstream gene, miR-766, was
assessed, and their co-regulation on primary lung carcinoma was determined by rescue experiments.
Results: CircZNF652 was abnormally and significantly upregulated in primary lung carcinoma cases (p< 0.05), resulting in a poor prognosis. The knockdown effect of circZNF652 attenuated the proliferative and migratory capacities of A549 and SPC-A-1 cells, and downregulated epithelial-mesenchymal transition (EMT)-associated genes. CircZNF652 bound and negatively regulated miR-766, a key
downstream gene involved in circZNF652-induced aggravation of primary lung carcinoma.
Conclusion: CircZNF652 serves as an oncogene, triggering the aggravation of primary lung carcinoma by negatively regulating miR-766. The results of this study may provide new insights into the treatment of lung carcinoma.