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目的研究长链非编码RNA(long non-coding RNA,lncRNA)HOXA末端转录本反义RNA(HOXA transcript at the distal tip,HOTTIP)对宫颈癌细胞增殖、迁移及侵袭能力的影响。方法将HOTTIP小干涉RNA(siRNA)及negative siRNA转染He La和C-33A宫颈癌细胞系,通过实时荧光定量PCR(q PCR)技术确认HOTTIP在细胞中表达水平的敲低,采用CCK8及克隆形成实验检测HOTTIP降低表达后对He La和C-33A细胞增殖的影响,细胞划痕实验检测HOTTIP降低表达后对He La和C-33A细胞增殖及迁移能力的影响,Matrigel细胞侵袭实验检测HOTTIP降低表达后对He La及C-33A侵袭能力的影响。结果向宫颈癌细胞系He La和C-33A中转染HOTTIP siRNA 48 h后,经q PCR检测He La及C-33A细胞中HOTTIP均出现明显下调;CCK8及克隆形成实验结果显示,HOTTIP降低表达能显著抑制He La及C-33A细胞的增殖(P<0.01);细胞划痕实验结果显示,HOTTIP降低表达能减弱He La和C-33A细胞增殖及迁移能力;Matrigel细胞侵袭实验结果显示,HOTTIP降低表达能减弱He La及C-33A侵袭能力。结论HOTTIP siRNA转染He La及C-33A宫颈癌细胞系能有效降低HOTTIP的表达,同时HOTTIP降低表达后能抑制宫颈癌细胞的增殖、迁移和侵袭能力。
Objective To investigate the effect of long non-coding RNA (HOXA transcript at the distal tip, HOTTIP) on the proliferation, migration and invasion of cervical cancer cells. Methods HOTTIP small interfering RNA (siRNA) and negative siRNA were transfected into HeLa and C-33A cervical cancer cell lines. The expression of HOTTIP was knocked down by real-time quantitative PCR (qPCR) The effect of HOTTIP on the proliferation and migration of HeLa and C-33A cells was detected by the cell scratch assay. The decrease of HOTTIP was detected by Matrigel invasion assay Effect of Expression on Invasion Ability of He La and C-33A. Results HOTTIP siRNA was transfected into HeLa and C-33A cervical cancer cell lines for 48 h, and the expression of HOTTIP was significantly down-regulated in HeLa and C-33A cells by q PCR. The results of CCK8 and clonogenic assay showed that HOTTIP reduced expression (P <0.01). The results of cell scratch assay showed that the decrease of the expression of HOTTIP attenuated the proliferation and migration of He La and C-33A cells. The results of Matrigel cell invasion assay showed that HOTTIP Decreased expression attenuated He La and C-33A invasiveness. Conclusion HOTTIP siRNA transfected He La and C-33A cervical cancer cell lines can effectively reduce the expression of HOTTIP, while the expression of HOTTIP siRNA can inhibit the proliferation, migration and invasion of cervical cancer cells.