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.
[1] 董小琳,柳志文.LC3B和mTOR在口腔黏膜白斑和口腔鳞癌组织中的表达[J].实用口腔医学杂志,2019,35(3):403-407. [2] 俞晴,静广平,顾玉洲,等.SRSF1和Survivin在口腔鳞状细胞癌中的表达及临床意义[J].现代生物医学进展,2019,19(3):490-493. [3] Aanhold C,Bus P,Zandbergen M,et al.The vascular endothelial growth factor inhibitor soluble FLT-1 ameliorates atopic dermatitis in APOC1 transgenic mice-science direct[J].Journal of Investigative Dermatology,2020,140( 2):491-494. [4] 李月洁,周铁军,刘艳,等.口腔鳞癌组织CD133、血管内皮生长因子C的表达变化及其意义[J].山东医药,2019,59(6):59-62. [5] Lu Z,Li Y,Wang J,et al.Long non-coding RNA NKILA inhibits migration and invasion of non-small cell lung cancer via NF-κB/Snail pathway[J].Journal of Experimental & Clinical Cancer Research,2017,36(1):54. [6] 樊超.miR-3195对人喉癌Hep-2细胞增殖的抑制作用及其机制研究[D].南华大学,2016. [7] Tibatan M A, Uar E N.Long non-coding RNA NKILA regulates expression of HSP90α,NF-κB and β-catenin proteins in the MCF-7 breast cancer cell line[J].Molecular Biology Reports,2021,48(5):4563-4571. [8] 雷梓巍,陈艳华,樊超,等.miR-3195对人喉癌Hep-2细胞增殖的抑制作用及其机制[J].中国肿瘤生物治疗杂志,2020,27(12):1372-1377. [9] Jiang X, Gao Z, Tian L,et al.Expressions of miR-122a and miR-3195 in laryngeal cancer and their effects on the proliferation and apoptosis of laryngeal cancer cell Hep-2[J].Advances in Clinical and Experimental Medicine,2020,29(5):525-534 [10] 张旭,刘佳文.MMP-9,COX-2,NF-κB在口腔鳞状细胞癌组织中的表达及意义[J].口腔医学研究,2021,37(4):360-365. [11] 戴红良,葛树卿,楚明会.染料木黄酮通过抑制VEGF表达抑制人口腔癌TCA8113细胞增殖[J].中国病理生理杂志,2016,32(3):464-469. [12] Sohn E J, Won G, Lee J,et al.Upregulation of miRNA3195 and miRNA374b mediates the anti-angiogenic properties of melatonin in hypoxic PC-3 prostate cancer cells[J].Journal of Cancer,2015,6(1):19-28.