MiR-16 inhibits proliferation of cervical cancer cells by regulating KRAS

Z. Ding, S.-J. Liu, X.-W. Liu, Q. Ma, Z. Qiao

Department of Oncology, Affiliated Hospital of Jining Medical University, Jining, Jining, China. qz227@126.com

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• Oncology

OBJECTIVE: The aim of this study was to explore the effects of micro ribonucleic acid (miR)-16 on the proliferation and apoptosis of cervical cancer (CC) cells and its related regulatory mechanism.

MATERIALS AND METHODS: The downstream regulatory targets of miR-16 were analyzed based on the miRNA online database. HCC94 cells were selected as experimental objects. Subsequently, the cells were transfected with miR-16 mimic (miR-16 mimic group), miR-16 small interfering RNA (siRNA) (miR-16 siRNA group) and only Lipofectamine 2000 transfection reagent [blank control group and miR-16 normal control (NC) group]. The expression level of miR-16 in HCC94 cells was measured via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay, 5-Ethynyl-2’-deoxyuridine (EdU) staining assay and flow cytometry were then conducted to detect the effects of miR-16 on the viability, proliferation and apoptosis of HCC94 cells, respectively. Additionally, the effect of miR-16 on the protein expression level of Kirsten rat sarcoma viral oncogene homolog (KRAS) in HCC94 cells was determined via Western blotting.

RESULTS: MiRNA online database analysis showed that KRAS was the downstream target of miR-16. Compared with miR-16 NC group, the viability and proliferation ability of HCC94 cells increased significantly in miR-16 siRNA group but decreased significantly in miR-16 mimic group (p<0.05). However, the apoptosis rate evidently declined in miR-16 siRNA group while increased remarkably in miR-16 mimic group (p<0.05). In addition, the protein expression level of KRAS in HCC94 cells was significantly higher in miR-16 siRNA group but significantly lower in miR-16 mimic group when compared with miR-16 NC group (p<0.05).

CONCLUSIONS: MiR-16 is lowly expressed in HCC94 cells. Moreover, highly expressed miR-16 represses the viability and proliferation of HCC94 cells and promotes their apoptosis by targeted regulation on KRAS.

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