LncRNA-NKILA靶向miR-3195对口腔癌细胞活性及血管生成的作用机制

doi:10.3969/j.issn.1006-6233.2022.10.02

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Abstract Objective: To investigate the effect of lncrNA-NKILA targeting miR-3195 on the activity and angiogenesis of oral cancer cells. Methods: The expression levels of LncRNA-NKILA in human normal oral epithelial cells and human oral squamous carcinoma cells were measured by qRT-PCR.According to the random number table method,they were divided into empty plasmid group (SCC25 cell line + pcDNA),NEAT1 group (SCC25 cell line + pcDNA-NKILA),NC-group (SCC25 cell line + miR-3195-NC-mimics); miR-3195 group (SCC25 cell line + miR-3195-mimics),and Combination 1 group (SCC25 cell line + pcDNA-NKILA + miR-3195-NC-mimics) and Combination 2 group (SCC25 cell line + pcDNA-NKILA + miR-3195-mimics).Cell proliferation was detected by CCK-8 method; apoptosis rate was detected by flow cytometry,VEGF and VEGF-C proteins were detected by immunoblotting; and miR-3195 regulation by LncRNA-NKILA was detected by luciferase method. Results: SCC25 cell lines transfected with pcDNA-NKILA showed decreased cell proliferation,increased apoptosis,and decreased VEGF and VEGF-C proteins,compared with the empty plasmid group (P<0.05); compared with the NC group,SCC25 cell lines in the miR-3195 group showed decreased proliferation,increased apoptosis,and decreased VEGF and VEGF-C proteins (P<0.05).The proliferation of SCC25 cell lines was reduced,apoptosis rate was increased,and VEGF and VEGF-C proteins were reduced in the combination 2 group compared with the combination 1 group (P<0.05); luciferase assay showed that miR-3195 was a LncRNA-NKILA target gene. Conclusion: LncrNA-NKILa can inhibit the proliferation of oral cancer cells and promote their apoptosis by regulating the expression of miR-3195,and the study mechanism may be related to the inhibition of VEGF expression.

Key words： Oral squamous cell carcinoma Long non-coding RNA NKILA MiR - 3195 Vascular endothelial growth factor

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2022.10.02 OR http://www.hbyxzzs.cn/EN/Y2022/V28/I10/1591

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