| 陈斌,王猛,张囡囡.长链非编码 RNA组蛋白去乙酰化酶 3通过哺乳动物雷帕霉素靶蛋白信号通路调控肝癌细胞增殖、迁移侵袭和凋亡[J].安徽医药,2021,25(9):1775-1779. |
| 长链非编码 RNA组蛋白去乙酰化酶 3通过哺乳动物雷帕霉素靶蛋白信号通路调控肝癌细胞增殖、迁移侵袭和凋亡 |
| Long-chain non-coding RNA HDAC3 regulates hepatocellular carcinoma cell proliferation, migration, invasion and apoptosis via mTOR signaling pathway |
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| DOI：10.3969/j.issn.1009-6469.2021.09.018 |
| 中文关键词: 肝肿瘤 蛋白质丝氨酸苏氨酸激酶 细胞增殖 细胞运动 肿瘤侵润 细胞凋亡 长链非编码 RNA组蛋白去乙酰化酶 3 哺乳动物雷帕霉素靶蛋白信号通路 |
| 英文关键词: Liver neoplasms Protein-serine-threonine kinases Cell proliferation Cell movement Neoplasm invasiveness Apoptosis Long-chain non-coding RNA HDAC3 Mammalian target of rapamycin signaling pathway |
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| 中文摘要: |
| 目的研究长链非编码 RNA组蛋白去乙酰化酶 3(HDAC3)对肝癌细胞增殖、迁移、侵袭和凋亡的调控机制。方法运用实时荧光定量逆转录聚合酶链反应( qRT-PCR)检测正常肝细胞 MIHA、肝细胞癌细胞 SK-Hep1中 HDAC3的表达；将 si-NC组(转染 si-NC)、 si-HDAC3组(转染 si-HDAC3)、 si-HDAC3+DMSO组［转染 si-HDAC3并用二甲基亚砜( DMSO)处理］、 si-HDAC3+ MHY1485组［转染 si-HDAC3并用哺乳动物雷帕霉素靶蛋白( mTOR)信号通路抑制剂 MHY1485处理］用脂质体法转染至 SKHep1细胞； CCK-8法检测细胞增殖； Transwell小室检测细胞迁移侵袭；流式细胞术检测细胞凋亡；蛋白质印迹法( Western blotting)检测细胞中 Akt激酶、翻译起始因子 4E结合蛋白 1(4E-BP1)、核糖体 p70S6激酶蛋白( S6K1)、磷酸化核糖体 p70S6激酶蛋白( p-S6K1)的蛋白表达。结果与正常肝细胞 MIHA(1.00±0.06)相比，肝细胞癌细胞 SK-Hep1中 HDAC3表达( 4.38±0.34)显著上调( P<0.05)。敲减 HDAC3后， SK-Hep1细胞的增殖、迁移、侵袭能力均得到明显下调，凋亡能力得到明显上调。有趣的是，敲减 HDAC3后， SK-Hep1细胞中 mTOR信号通路关键基因 Akt、4E-BP1、p-S6K1的表达均明显下调，并且激活 mTOR信号通路可部分逆转敲减 HDAC3对肝癌细胞的增殖、迁移、侵袭和凋亡调控作用。结论长链非编码 RNA HDAC3可调控肝癌细胞的增殖、迁移、侵袭和凋亡，其机制可能与 mTOR信号通路相关，可为肝癌的治疗提供新的作用靶点。 |
| 英文摘要: |
| Objective To study the regulation mechanism of long-chain non-coding RNA HDAC3 on proliferation, migration, invasion and apoptosis of hepatocellular carcinoma cells.Methods qRT-PCR was used to detect the expression of HDAC3 in normal liver cells MIHA and hepatocellular carcinoma cell line SK-Hep1. si-NC group (transfected with si-NC), si-HDAC3 group (transfected with si-HDAC3), si-HDAC3+DMSO group [transfected with si-HDAC3 and treated with dimethyl sulfoxide (DMSO)], si-HDAC3+MHY1485 group [transfected with si-HDAC3 and treated with mammalian target of rapamycin (mTOR) signaling pathway inhibitors MHY1485] transfected into SK-Hep1 cells by liposome method; cell proliferation was detected by CCK-8 method; cell migration and invasion weredetected by Transwell chamber; apoptosis was detected by flow cytometry; protein expression of Akt, translation initiation factor 4Ebinding protein 1(4E-BP1), ribosome p70S6 kinase protein (S6K1), phosphorylated ribosome p70S6 kinase protein(p-S6K1) were detected by Western blotting.Results Compared with normal liver cell MIHA (1.00±0.06), HDAC3 expression (4.38±0.34) was significantly up-regulated in hepatocellular carcinoma cell line SK-Hep1 (P< 0.05). After knocking down HDAC3, the proliferation, migration and invasion of SK-Hep1 cells were significantly down-regulated, and the apoptosis ability was significantly up-regulated. Interestingly, the expression of the key genes of Akt, 4E-BP1 and p-S6K1 in SK-Hep1 cells was down-regulated after knockdown of HDAC3. Activationof mammalian target of rapamycin (mTOR) signaling pathway partially reversed the regulation of proliferation, migration, invasion andapoptosis of hepatocellular carcinoma cells by knockdown HDAC3.Conclusion Long-chain non-coding RNA HDAC3 can regulatethe proliferation, migration, invasion and apoptosis of hepatocarcinoma cells, and its mechanism may be related to mTOR signalingpathway, which will provide a new target for the treatment of hepatocellular carcinoma. |
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