| 陈素华,马天江,张智慧,等.长链非编码 RNA LINC01419调控结直肠癌细胞增殖、凋亡、迁移侵袭的机制[J].安徽医药,2022,26(3):572-577. |
| 长链非编码 RNA LINC01419调控结直肠癌细胞增殖、凋亡、迁移侵袭的机制 |
| The mechanism by which the long noncoding RNA LINC01419 regulates colorectal cancer cell proliferation, apoptosis and migration and invasion |
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| DOI：10.3969/j.issn.1009-6469.2022.03.036 |
| 中文关键词: 结直肠肿瘤 长链非编码 RNA LINC01419 微小 RNA-132-3p 增殖 凋亡 |
| 英文关键词: Colorectal neoplasms LncRNA LINC01419 MiR-132-3p Proliferation Apoptosis |
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| 中文摘要: |
| 目的研究长链非编码 RNA(lncRNA)LINC01419调控结直肠癌细胞增殖、凋亡、迁移侵袭的机制。方法收集漯河市中心医院 2015年 10月至 2018年 5月因结直肠癌手术切除的组织标本 20例，以距离结直肠癌边缘 ≥3 cm的癌旁正常组织标本 20例为对照。实时荧光定量逆转录聚合酶链反应( qRT-PCR)检测结直肠癌组织中 lncRNA LINC01419和微小 RNA-132-3p(miR-132-3p)表达。构建干扰 lncRNA LINC01419或 miR-132-3p过表达的结直肠癌 SW620细胞， MTT法和流式细胞术分别检测细胞增殖与凋亡， Transwell检测细胞迁移、侵袭，蛋白质印迹法( Western blotting)检测细胞周期蛋白 D1(cyclin D1)、细胞周期蛋白依赖性激酶抑制剂 1A(P21)、 B细胞淋巴瘤 -2(Bcl-2)蛋白、 Bcl-2相关 X(Bax)蛋白、基质金属蛋白酶 -2(MMP-2)、基质金属蛋白酶 -9(MMP-9)蛋白表达。生物信息学预测结合双荧光素酶报告实验分析 lncRNA LINC01419和 miR-132-3p的靶向关系。 si-LINC01419和 anti-miR-123-3p共转染，观察抑制 miR-132-3p表达对干扰 lncRNA LINC01419诱导的 SW620细胞增殖、凋亡、迁移、侵袭的影响。结果与癌旁组织［(1.00±0.09)、(1.01±0.08)］比较，结直肠癌组织中 lncRNA LINC01419表达量( 2.74± 0.26)明显增加( P<0.05)miR-132-3p表达量( 0.51±0.05)显著减少( P<0.05)。干扰 lncRNA LINC01419或 miR-132-3p过表达显著抑制 SW620细胞增殖、，迁移、侵袭、 cyclin D1、Bcl-2、MMP-2、MMP-9蛋白表达，并促进细胞凋亡、 P21、Bax蛋白表达。 lncRNA LINC01419靶向调控 miR-132-3p的表达。抑制 miR-132-3p表达逆转了干扰 lncRNA LINC01419对结直肠癌细胞 SW620增殖、迁移、侵袭的抑制作用，以及对细胞凋亡的促进作用。结论 lncRNA LINC01419通过靶向 miR-132-3p调控结直肠癌细胞增殖、凋亡、迁移侵袭。 |
| 英文摘要: |
| Objective To study the mechanism by which the long noncoding RNA (lncRNA) LINC01419 regulates colorectal cancercell proliferation, apoptosis, migration and invasion.Methods Twenty tissue samples from Luohe Central Hospital from October 2015to May 2018 due to surgical resection of colorectal cancer were collected, and 20 normal tissue samples with a distance of ≥3 cm fromthe edge of colorectal cancer were used as controls. qRT-PCR was used to detect the expression of lncRNA LINC01419 and microRNA132-3p (miR-132-3p) in colorectal cancer tissues. After construction of lncRNA LINC01419-silenced or miR-132-3p-overexpressingcolorectal cancer SW620 cells, MTT assay and flow cytometry were applied to detect cell proliferation and apoptosis, Transwell assayswere employed to detect cell migration and invasion, and Western blotting was used to analyze cyclin D1, cyclin-dependent kinase inhibitor 1A (P21), B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), matrix metalloproteinase-2 (MMP-2), and MMP-9 protein expression. Bioinformatics prediction combined with a dual luciferase reporter assay was used to analyze the targeting relationshipbetween lncRNA LINC01419 and miR-132-3p. Si-LINC01419 and anti-miR-123-3p were cotransfected to observe the effect of inhibiting miR-132-3p on the proliferation, apoptosis, migration and invasion of SW620 cells induced by lncRNA LINC01419 silencing.Re? sults Compared with the adjacent tissues [(1.00±0.09), (1.01±0.08)], the expression of lncRNA LINC01419 (2.74±0.26) in colorectalcancer tissues was significantly increased (P<0.05), while the expression of miR-132-3p (0.51±0.05) was obviously decreased (P<0.05). Silencing lncRNA LINC01419 or overexpressing miR-132-3p markedly inhibited SW620 cell proliferation, migration and invasion and cyclin D1, Bcl-2, MMP-2, and MMP-9 protein expression and promoted apoptosis and P21 and Bax protein expression. The lncRNA LINC01419 targets miR-132-3p. Inhibition of miR-132-3p reversed the inhibitory effects of interfering with lncRNA LINC01419 on the proliferation, migration and invasion of SW620 colorectal cancer cells, as well as the promotion of apoptosis.Conclusion The lncRNA LINC01419 regulates colorectal cancer cell proliferation, apoptosis, migration and invasion by targeting miR-132-3p. |
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