| 谭建福,饶丽娟,王秀.长链非编码 RNA肝癌高表达转录本通过微小 RNA-134-5p促进宫颈癌细胞恶性生物学行为的机制研究[J].安徽医药,2022,26(10):2044-2049. |
| 长链非编码 RNA肝癌高表达转录本通过微小 RNA-134-5p促进宫颈癌细胞恶性生物学行为的机制研究 |
| LncRNA HULC promotes the malignant biological behavior of cervical cancer cells through miR-134-5p |
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| DOI：10.3969/j.issn.1009-6469.2022.10.032 |
| 中文关键词: 宫颈肿瘤 长链非编码 RNA肝癌高表达转录本 miR-134-5p 增殖 凋亡 侵袭 迁移 |
| 英文关键词: Uterine cervical neoplasms lncRNA HULC miR-134-5p Proliferation Apoptosis Invasion Migrate |
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| 中文摘要: |
| 目的探讨长链非编码 RNA(lncRNA)肝癌高表达转录本( HULC)通过抑制微小 RNA-134-5p促进宫颈癌细胞增殖、袭和迁移，促进凋亡的作用及其作用机制。方法 2019年 10月至 2020年 5月，通过实时荧光定量 PCR(qRT-PCR)检测体外培侵养的人正常宫颈上皮细胞和宫颈癌细胞中 HULC的表达情况，在宫颈癌 C-33A细胞中转染特异性 HULC siRNA，qRT-PCR检测转染效果，细胞计数试剂盒( CCK-8)法分析 C-33A细胞增殖情况，采用流式细胞术分析 C-33A细胞凋亡情况， Transwell实验分析 C-33A细胞侵袭和迁移能力，双荧光素酶报告基因实验检测 HULC与 miR-134-5p的相互作用。在抑制 HULC表达的 C-33A细胞中转染 miR-134-5p抑制剂，以同样的方法检测对细胞增殖、侵袭和迁移的影响。结果 HULC在宫颈癌细胞( HeLa、Cas. ki、SiHa、C-33A)中的表达水平为(1.95±0.24、2.26±0.21、1.77±0.19、3.49±0.40)，显著高于正常宫颈上皮细胞 1.00±0.11，HULC在 C-33A细胞中的表达量最高( P<0.05)。转染特异性 HULC siRNA能够抑制 C-33A细胞中 HULC的表达( 0.94±0.08比 0.18± |
| 英文摘要: |
| Objective To explore the role and mechanism of long non-coding RNA (lncRNA) highly upregulated in liver cancer (HULC) by inhibiting miR-134-5p in promoting the proliferation, invasion and migration of cervical cancer cells and promoting apopto. sis.Methods From October 2019 to May 2020, the expression of HULC in human normal cervical epithelial cells and cervical cancercells cultured in vitro was detected by real-time fluorescent quantitative PCR (qRT-PCR). Specific HULC siRNA was transfected into cervical cancer C-33A cells, and the transfection effect was detected by qRT-PCR. CCK-8 method was adopted to analyze the prolifera. tion of C-33A cells, flow cytometry to analyze the apoptosis of C-33A cells, and Transwell experiment to analyze the invasion and migra. tion ability of C-33A cells. The dual luciferase reporter gene assay detected the interaction of HULC with miR-134-5p. The miR-134-5p inhibitors were transfected into C-33A cells that inhibited HULC expression, and the effects on cell proliferation, invasion and mi.gration were examined in the same manner.Results The expressions of HULC in cervical cancer cells (HeLa, Caski, SiHa, C-33A)were 1.95±0.24, 2.26±0.21, 1.77±0.19, 3.49±0.40, respectively, which were significantly higher than that in normal cervical epithelialcells, (1.00±0.11). The expression of HULC was the highest in C-33A cells (P<0.05). Transfection-specific HULC siRNA was able to in. hibit HULC expression (0.94±0.08 vs. 0.18±0.02) in C-33A cells. After inhibiting the expression of HULC, the OD value of C-33A cells was decreased (0.59±0.08 vs. 0.38±0.05), the apoptotic rate was significantly increased [(3.01±0.34) % vs. (18.54±2.16) %], and the in. vasion (112.54±13.86 vs. 46.28±10.16) and migration (158.65±18.66 vs. 78.18±10.80) ability was weakened (P<0.05). HULC was able to specifically bind to miR-134-5p and negatively regulate the expression of miR-134-5p. Inhibition of miR-134-5p expression reversed the inhibition of HULC-induced C-33A cell proliferation, apoptosis, invasion and migration.Conclusion HULC promotes the prolifer. ation, invasion and migration of cervical cancer cells by inhibiting the expression of miR-134-5p, and induces apoptosis. |
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