| 常晓苗.长链非编码小核仁 RNA宿主基因 7调控微小 RNA-331-3p表达影响甲状腺癌细胞增殖、迁移和侵袭的机制研究[J].安徽医药,2021,25(10):2088-2092. |
| 长链非编码小核仁 RNA宿主基因 7调控微小 RNA-331-3p表达影响甲状腺癌细胞增殖、迁移和侵袭的机制研究 |
| Mechanism of long non-coding small nucleolar RNA host gene 7 (lncRNA SNHG7) regulating the expression of microRNA-331-3p (miR-331-3p) and affecting proliferation, migration and invasion of thyroid carcinoma cells |
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| DOI：10.3969/j.issn.1009-6469.2021.10.042 |
| 中文关键词: 甲状腺肿瘤 RNA，长链非编码 RNA，小核仁 长链非编码小核仁 RNA宿主基因 7 miR-331-3p 增殖 迁移 侵袭 |
| 英文关键词: Thyroid neoplasms RNA,long noncoding RNA,small nucleolar SNHG7 MiR-331-3p Proliferation Migration Invasion |
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| 中文摘要: |
| 目的探讨长链非编码小核仁 RNA宿主基因 7(lncRNA SNHG7)对甲状腺癌细胞增殖、迁移和侵袭的影响以及潜在的作用机制。方法本研究起止时间为 2018年 1月至 2019年 2月，人甲状腺细胞 Nthy-ori 3-1和人甲状腺癌细胞 K1、BCPAP、 TPC-1购自中国科学院上海细胞库，用 qRT-PCR检测 SNHG7和微小 RNA-331-3p(miR-331-3p)的表达水平；将 si-NC组(转染 SNHG7干扰表达载体阴性对照)、 si-SNHG7组(转染 SNHG7干扰表达载体)、 si-SNHG7+anti-miR-NC组(共转染 SNHG7干扰表达载体和 miR-331-3p抑制剂阴性对照)、 si-SNHG7+anti-miR-331-3p组(共转染 SNHG7干扰表达载体和 miR-331-3p抑制剂)，均用脂质体法转染至 TPC-1细胞；采用蛋白质印迹法( Western Blotting)检测蛋白表达；四甲基偶氮唑盐比色法( MTT)检测细胞增殖； Transwell检测细胞迁移和侵袭；双荧光素酶报告基因检测实验检测荧光活性。结果与人甲状腺细胞 Nthy-ori 3-1相比，人甲状腺癌细胞 K1、BCPAP、TPC-1中 SNHG7的表达水平显著升高［( 1.42±0.16)、(1.51±0.18)、(2.56±0.15)比( 1.01±0.05)］； miR-331-3p的表达水平显著下降［( 0.63±0.11)、(0.60±0.10)、(0.42±0.08)比( 1.00±0.06)］，差异有统计学意义( P<0.05)。与 siNC组相比， si-SNHG7组 TPC-1细胞中细胞周期蛋白 D1(Cyclin D1)、神经钙黏蛋白( N-cadherin)的表达水平显著降低，细胞周期蛋白依赖性激酶抑制剂 1A(p21)、上皮钙黏蛋白( E-cadherin)的表达水平显著升高， TPC-1细胞活性显著降低［24 h:(0.20±0.06)比( 0.49±0.10)，48 h:(0.50±0.13)比( 1.10±0.22)72 h:(0.60±0.13)比( 1.60±0.10)］迁移细胞数降低［(63±8.97)个比( 144±11.36)个］侵袭细胞数降低［(55±10.03)个比(136±138)个］差异有统计学意义(P<0)。 SNHG7可靶向调控 miR-331-3p的iR-331-3p表达可逆转干扰 SNHG7对 TPC-1细作用。 SNHG7可靶向调控 miR-331-3p的表达。抑制 miR-3313p表达可逆转干扰 SNHG7对 TPC-1细胞的作用。结论 干扰 SNHG7可通过上调 miR-331-3p抑制 TPC-1细胞的恶性生物学行为。 |
| 英文摘要: |
| Objective To explore the effects of long non-coding small nucleolar RNA host gene 7 (lncRNA SNHG7) on the proliferation, migration and invasion of thyroid cancer cells and its potential mechanism.Methods From January 2018 to February 2019, human thyroid cells Nthy-ori 3-1 and human thyroid cancer cells K1, BCPAP, and TPC-1 were purchased from the Shanghai Cell Bank of the Chinese Academy of Sciences; qRT-PCR was used to detect the expression levels of SNHG7 and microRNA-331-3p (miR-331-3p); the si-NC group (transfected with SNHG7 interference expression vector negative control), si-SNHG7 group (transfected with SNHG7 interference expression vector), si-SNHG7+anti-miR-NC group (co-transfected with SNHG7 interference expression vector and miR331-3p inhibitor negative control), si-SNHG7+anti-miR-331-3p group (co-transfected SNHG7 interference expression vector and miR331-3p inhibitor), both were transfected into TPC-1 cells by liposome method; protein expression was detected by Western blottingmethod; tetramethylazolium salt colorimetry method (MTT) to detect cell proliferation; Transwell was used to detect cell migration andinvasion; dual luciferase reporter gene assay was used to detect fluorescence activity.Results Compared with human thyroid cells Nthy-ori 3-1, the expression levels of SNHG7 in human thyroid cancer cells K1, BCPAP, and TPC-1 were significantly increased [(1.42±0.16), (1.51±0.18), (2.56±0.15) vs. (1.01±0.05)]; the expression level of miR-331-3p were significantly decreased [(0.63±0.11), (0.60±0.10), (0.42±0.08) vs. (1.00±0.06)], the difference was statistically significant (P<0.05). Compared with the si-NC group, the ex |
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