LincRNA-P21 通过靶向 miR-17-3p 对三阴性乳腺癌细胞 迁移和侵袭能力的影响. (Chinese)

Objective To investigate the effect of LincRNA-P21 on the migration and invasion of triple negative breast cancer (TNBC) cells by targeting miR-17-3p. Methods qPCR was used to detect the expression levels of LincRNA-P21 and miR-17-3p in tumor tissues, normal adjacent tissues and 6 kinds of breast cells (normal breast cells MCF-10A, breast cancer cells MDA-MB-231, MDA-MB-435, MDA-MB-468, BT549 and T47D). MDA-MB-231 cells were taken. LincRNA-P21 was overexpressed alone (the control group, the pcDNA3.1 blank group and the pcDNA - LincRNA-P21 group), miR-17-3p expression was inhibited (the control group, the miR-17-3p blank group and the miR-17-3p inhibitor group), and overexpression LincRNA-P21+ inhibited miR-17-3p (the control group, the miR-17-3p inhibitor group and the pcDNA-LincRNA-P21+miR-17-3p inhibitor group). The proliferation of MDA-MB-231 cells was detected by CCK-8 assay. The number of colonies was detected by colony formation assay. The migration ability was detected by cell scratch assay, and the invasion ability was detected by Transwell assay. The protein expressions of E-cadherin and Vimentin were detected by Western blot assay. Results The expression of LincRNA-P21 was significantly lower in TNBC than that in adjacent tissues (0.48±0.03 vs. 1.03±0.06, t=11.714, P＜0.01). The expression of miR-17-3p was significantly higher in TNBC than that in adjacent tissues (2.93±0.17 vs. 1.02±0.04, t=15.593, P＜0.01). The expression levels of LincRNA-P21 mRNA in different breast cancer cell lines were significantly lower than that in MCF-10A (P＜0.01). The expressions of miR-17-3p mRNA in different breast cancer cell lines were significantly higher than that in MCF-10A (P＜0.01). The overexpression of LincRNA-P21 inhibited cell proliferation, colony formation and invasion (P＜0.01). The inhibition of miR17-3p expression could reduce cell proliferation, colony formation and invasion (P＜0.01). Compared with the miR-NC group, the overexpression of LincRNA-P21 and inhibition of miR-17-3p could significantly reduce cell proliferation, colony formation and invasion (P＜0.01), increase the expression of E-cadherin and inhibit the expression of vimentin (P＜0.01). Conclusion LincRNA-P21 can reduce miR-17-3p expression and inhibit MDA-MB-231 cell proliferation, colony formation, migration and invasion through competitive binding. [ABSTRACT FROM AUTHOR]

目的 探讨 LincRNA-P21 通过靶向 miR-17-3p 对三阴性乳腺癌（TNBC）细胞迁移和侵袭作用的影响。方 法 qPCR检测30例TNBC患者肿瘤组织、癌旁正常组织以及 6 种乳腺细胞（乳腺正常细胞 MCF-10A，乳腺癌细胞 MDA-MB-231、MDA-MB-435、MDA-MB-468、BT549、T47D）LincRNA-P21和 miR-17-3p 的表达。取MDA-MB-231 细胞，单独过表达 LincRNA-P21（实验设对照组、pcDNA3.1空白组、pcDNA-LincRNA-P21组），抑制 miR-17-3p 表达 （实验设对照组、miR-17-3p空白组、miR-17-3p 抑制剂组），过表达LincRNA-P21+抑制miR-17-3p表达（实验设对照 组、miR-17-3p 抑制剂组和 pcDNA-LincRNA-P21+miR-17-3p inhibitor 组）。CCK-8 法检测 MDA-MB-231 细胞增殖， 集落形成实验检测细胞的集落数量，细胞划痕实验检测细胞的迁移能力，Transwell实验检测细胞侵袭能力。Western blot 检测E-cadherin和Vimentin蛋白表达。结果 TNBC患者组织中LincRNA-P21的表达明显低于癌旁组织（0.48± 0.03 vs. 1.03±0.06，t=11.714，P＜0.01），miR-17-3p 的表达显著高于癌旁组织（2.93±0.17 vs. 1.02±0.04，t=15.593，P＜ 0.01）。乳腺癌细胞系中 LincRNA-P21 表达量明显低于MCF-10A，miR-17-3p表达量高于 MCF-10A（P＜0.01）。单 独过表达 LincRNA-P21 或抑制 miR-17-3p 后，MDA-MB-231细胞增殖能力、集落形成数量、迁移和侵袭能力均明显 下降。过表达 LincRNA-P21 的同时抑制 miR-17-3p，MDA-MB-231 细胞增殖能力、集落形成数量、迁移和侵袭能力 出现进一步下降，且上调E-cadherin的表达，抑制Vimentin的表达（P＜0.05）。结论 LincRNA-P21 通过竞争性结合 miR-17-3p 来抑制 MDA-MB-231 细胞增殖、集落形成、迁移和侵袭。 [ABSTRACT FROM AUTHOR]

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