Long noncoding RNA MACC1‑AS1 is a potential sponge of microRNA‑34a in cervical squamous cell carcinoma and upregulates cyclin‑dependent kinase 6
- Jieqiong Jin
- Xuemei Chen
- Jing Chen
- Xin Geng
Affiliations: Department of Gynaecology, Qingdao Jiaozhou Central Hospital, Qingdao, Shandong 266300, P.R. China, Department of Obstetrics and Gynecology, Wuhan Third Hospital (Tongren Hospital of Wuhan University), Wuhan, Hubei 430060, P.R. China, Department of Gynecological Oncology, Qingdao Center Medical Group, Qingdao, Shandong 266042, P.R. China, Department of Gynaecology, Qingdao No. 6 People's Hospital, Qingdao, Shandong 266033, P.R. China
- Published online on: January 24, 2020 https://doi.org/10.3892/ol.2020.11346
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The present study aimed to investigate the role of long noncoding RNA MACC1‑AS1 in cervical squamous cell carcinoma (CSCC). In the present study MACC1‑AS1 expression as analyzed using reverse transcription‑quantitative PCR. The interactions between MACC1‑AS1 and miR‑34a was analyzed via overexpression experiments. Cell cycle and proliferation analyses were performed to analyze the roles of MACC1‑AS1 in regulating cancer cell cycle progression and cell proliferation. It was observed that MACC1‑AS1 was upregulated in CSCC, and its expression levels were elevated with the increase in clinical stage. Bioinformatics analysis revealed that MACC1‑AS1 may be a sponge of miR‑34a, which can target cyclin‑dependent kinase 6 (CDK6). In CSCC cells, MACC1‑AS1 overexpression led to upregulation of CDK6, while miR‑34a overexpression had the opposite effect and reduced the effects of MACC1‑AS1 overexpression in co‑transfected cells. Cell cycle and proliferation analyses demonstrated that MACC1‑AS1 and CDK6 promoted cell cycle progression and cell proliferation. By contrast, miR‑34a had the opposite effect on cell cycle proliferation and cell proliferation, reducing the effects induced by MACC1‑AS1 overexpression. Therefore, the lncRNA MACC1‑AS1 may serve as a sponge of miR‑34a to upregulate CDK6, thereby promoting cell cycle progression and cell proliferation.