Minfei Jin1, Lei Wang1, Tao Zheng1, Jun Yu1, Rong Sheng1, Hong Zhu2. 1. Department of Obstetrics and Gynecology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, YangPu District, Shanghai, China. 2. Department of Obstetrics and Gynecology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, YangPu District, Shanghai, China. Electronic address: zhuhong03@xinhuamed.com.cn.
Abstract
BACKGROUND: Cervical cancer (CC) is one of the most prevailing cancers among females. Accumulated studies concentrated on the regulatory role of micro RNA in cancers. This research is to explore the potential role of mir-195-3p in cervical cancer progression. METHODS: Bioinformatics tools were used to investigate differential expression of mir-195-3p and BCDIN3D in cervical cancer. RNA expression patterns of both mir-195-3p and BCDIN3D were detected by RT-PCR in CC cell lines. The protein expression of BCDIN3D was measured by Western Blot. Hela and Siha cell lines were transfected with mir-195-3p inhibitors, mir-195-3p mimics and BCDIN3D si-RNA, si-NC. Luciferase reporter assays were adopted to confirm the binding. The interplays between mir-195-3p and BCDIN3D were explored in CC cell lines. CCK-8 assays checked how mir-195-3p regulated cell proliferation and Ki67 was examined by Western blot for its protein expressions as a biomarker for CC cell proliferation. RESULTS: MiR-195-3p was downregulated while BCDIN3D was upregulated in cervical cancer cell lines. The binding was confirmed via Luciferase Assay. RT-PCR suggested that upregulation of mir-195-3p inhibited BCDIN3D and downregulation of BCDIN3D in return induced mir-195-3p. CCK-8 pointed out that overexpression of mir-195-3p inhibited the cell viability. Ki67 protein expression was inhibited by miR-195-3p mimics or silence of BCDIN3D. CONCLUSION: The present research led us to a conclusion that mir-195-3p might inhibit cervical cancer cell proliferation and was reversely regulated by BCDIN3D. This suggests that miR-195-3p mimics/ BCDIN3D si-RNA might be used in the treatments of cervical cancer in the future after various animal assays and clinical trials.
BACKGROUND: Cervical cancer (CC) is one of the most prevailing cancers among females. Accumulated studies concentrated on the regulatory role of micro RNA in cancers. This research is to explore the potential role of mir-195-3p in cervical cancer progression. METHODS: Bioinformatics tools were used to investigate differential expression of mir-195-3p and BCDIN3D in cervical cancer. RNA expression patterns of both mir-195-3p and BCDIN3D were detected by RT-PCR in CC cell lines. The protein expression of BCDIN3D was measured by Western Blot. Hela and Siha cell lines were transfected with mir-195-3p inhibitors, mir-195-3p mimics and BCDIN3D si-RNA, si-NC. Luciferase reporter assays were adopted to confirm the binding. The interplays between mir-195-3p and BCDIN3D were explored in CC cell lines. CCK-8 assays checked how mir-195-3p regulated cell proliferation and Ki67 was examined by Western blot for its protein expressions as a biomarker for CC cell proliferation. RESULTS:MiR-195-3p was downregulated while BCDIN3D was upregulated in cervical cancer cell lines. The binding was confirmed via Luciferase Assay. RT-PCR suggested that upregulation of mir-195-3p inhibited BCDIN3D and downregulation of BCDIN3D in return induced mir-195-3p. CCK-8 pointed out that overexpression of mir-195-3p inhibited the cell viability. Ki67 protein expression was inhibited by miR-195-3p mimics or silence of BCDIN3D. CONCLUSION: The present research led us to a conclusion that mir-195-3p might inhibit cervical cancer cell proliferation and was reversely regulated by BCDIN3D. This suggests that miR-195-3p mimics/ BCDIN3D si-RNA might be used in the treatments of cervical cancer in the future after various animal assays and clinical trials.