LncRNA NEAT1通过调节miR-506-5p/CFL2轴对人胃癌细胞增殖凋亡和侵袭的影响

doi:10.3969/j.issn.1006-6233.2023.03.012

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Abstract Objective: To investigate the regulation of long non-coding RNA nuclear-enriched abundant transcript 1 (lncRNA NEAT1) on the miR-506-5p/cofilin-2 (CFL2) axis, and its influences on the biological behaviors of gastric cancer cells such as proliferation, apoptosis, migration, and invasion. Methods: BGC-823 cells were cultured in vitro, and lncRNA NEAT1 low expression vector (si-NEAT1) and miR-506-5p inhibitor (miR-506-5p inhibitor) were transfected into BGC-823 cells, which were divided into the si-NC group, si-NEAT1 group, inhibitor NC group, miR-506-5p inhibitor NC group, si-NEAT1+miR-506-5p inhibitor NC group, and si-NEAT1+miR-506-5p inhibitor group. RT-qPCR was performed to determine the expression of lncRNA NEAT1 and miR-506-5p to determine the transfection efficiency. CCK-8 assay was performed to determine proliferation. Flow cytometry was performed to determine apoptosis; a Transwell assay was performed to determine migration and invasion. Western blot was performed to determine the protein expressions of CFL2 and cyclin-dependent kinase 4 (CDK4). Dual-luciferase validation assay was performed to validate the targeting relationship of lncRNA NEAT1, CFL2, and miR-506-5p; nude mouse tumor-bearing experiments were carried out to further verify the targeted regulation of lncRNA NEAT1, miR-506-5p, and CFL2. Results: Compared with the si-NC group, cell proliferation, invasion ability, and CFL2 expression in the si-NEAT1 group were decreased, while apoptosis rate and miR-506-5p expression were increased (P<0.05). Compared with the inhibitor NC group, cell proliferation, invasion ability, and CFL2 expression were increased in the miR-506-5p inhibitor group, while apoptosis rate and miR-506-5p expression were decreased (P<0.05). LncRNA NEAT1 could target and regulate the expression of miR-506-5p, and CFL2 was the target gene of miR-506-5p. Knockdown of miR-506-5p could weaken the anti-proliferation, anti-invasion, and pro-apoptosis effects of lncRNA NEAT1 low expression (P<0.05). miR-506-5p inhibitor attenuated the anti-graft tumor growth effect of lncRNA NEAT1 low expression (P<0.05). Overexpression of CFL2 attenuated the anti-graft tumor growth effect of overexpression of miR-506-5p (P<0.05). Conclusion: LncRNA NEAT1 can affect the biological behaviors such as proliferation, invasion, and apoptosis of human gastric cancer cells by targeting and regulating the miR-506-5p/CFL2 axis.

Key words： LncRNA NEAT1 MiR-506-5p Gastric cancer Proliferation Apoptosis

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2023.03.012 OR http://www.hbyxzzs.cn/EN/Y2023/V29/I3/412

[1] Petrillo A,Smyth E C.27 years of stomach cancer:painting a global picture[J].Lancet Gastroenterol Hepatol,2020,5(1):5-6.
[2] 刘玲,钟慧钰,陆小军,等.LncRNA在胃癌中的作用及机制研究进展[J].肿瘤预防与治疗,2020,33(7):612-618.
[3] Yang L,Wang M,He P.LncRNA NEAT1 promotes the progression of gastric cancer through modifying the miR-1224-5p/RSF1 signaling axis[J].Cancer Manag Res,2020,12(8):11845-11855.
[4] Azadeh M,Salehzadeh A,Ghaedi K,et al.NEAT1 can be a diagnostic biomarker in the breast cancer and gastric cancer patients by targeting XIST,hsa-miR-612,and MTRNR2L8:integrated RNA targetome interaction and experimental expression analysis[J].Genes Environ,2022,44(1):16-33.
[5] Chen G,Liao J,Xu Y,et al.LINC01232 promotes metastasis and EMT by regulating miR-506-5p/PAK1 axis in gastric cancer[J].Cancer Manag Res,2022,14(13):1729-1740.
[6] Nguyen M T,Min K H,Kim D,et al.CFL2 is an essential mediator for myogenic differentiation in C2C12 myoblasts[J].Biochem Biophys Res Commun,2020,533(4):710-716.
[7] Bian Y,Guo J,Qiao L,et al.miR-3189-3p mimics enhance the effects of S100A4 siRNA on the inhibition of proliferation and migration of gastric cancer cells by targeting CFL2[J].Int Mol Sci,2018,19(1):236-251.
[8] 季策,戴经纬,陈鑫瑩,等.干扰组织蛋白酶F表达对胃癌裸鼠肿瘤体内增殖能力的影响[J].中国临床研究,2020,33(7):16-20.
[9] Carlevaro-Fita J,Lanzos A,Feuerbach L,et al.Cancer LncRNA Census reveals evidence for deep functional conservation of long noncoding RNAs in tumorigenesis[J].Commun Biol,2020,3(1):56-66.
[10] Mai H,Xu H,Lin H,et al.LINC01541 functions as a ceRNA to Modulate the Wnt/β-catenin pathway by decoying miR-506-5p in endometriosis[J].Reprod Sci,2021,28(3):665-674.
[11] 李敏,赵妍丽,杜国波,等.宫颈癌组织lncRNA FOXD2-AS1、miR-506-5p表达变化及其临床意义[J].山东医药,2020,60(34):71-74.
[12] Nguyen M T,Lee W.miR-320-3p regulates the proliferation and differentiation of myogenic progenitor cells by modulating actin remodeling[J].Int Mol Sci,2022,23(2):801-822.
[13] Nguyen M T,Lee W.miR-141-3p regulates myogenic differentiation in C2C12 myoblasts via CFL2-YAP-mediated mechanotransduction[J].BMB Rep,2022,55(2):104-109.
[14] 杨满,吴隼,黄琰,等.miR-199调控CFL2蛋白表达对慢性粒细胞白血病细胞增殖和侵袭影响[J].中华肿瘤防治杂志,2018,25(7):466-470.