| 姚庆东,张福生,张国顺,等.miR-568通过下调 AKR1B10表达影响胶质母细胞瘤细胞的增殖和凋亡[J].安徽医药,2022,26(4):705-710. |
| miR-568通过下调 AKR1B10表达影响胶质母细胞瘤细胞的增殖和凋亡 |
| miR-568 affects the proliferation and apoptosis of glioblastoma cells by downregulating AKR1B10 expression |
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| DOI：10.3969/j.issn.1009-6469.2022.04.015 |
| 中文关键词: 胶质母细胞瘤 微小 RNA-568 醛酮还原酶家族 1成员 B10 细胞增殖 凋亡 |
| 英文关键词: Glioblastoma MiR-568 Aldosterone reductase family 1 member B10 Cell proliferation Apoptosis |
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| 中文摘要: |
| 目的探讨微小 RNA-568(miR-568)对胶质母细胞瘤细胞增殖和凋亡的影响及作用机制。方法培养正常星形胶质细胞 HA1800及胶质母细胞瘤细胞系( U251、T98G和 SHG44)购自中国科学院上海细胞库， qRT-PCR检测细胞中 miR-568和醛酮还原酶家族 1成员 B10(AKR1B10)mRNA表达，蛋白质印迹法( Western blotting)检测 AKR1B10蛋白表达。以 U251细胞为研究对象，构建上调 miR-568或下调 AKR1B10的 U251细胞， MTT、流式细胞仪和 Western blotting实验检测细胞增殖、凋亡及细胞中 CyclinD1、p21、Bcl-2和 Bax蛋白表达。双荧光素酶报告基因实验验证 miR-568与 AKR1B10调控关系。结果胶质母细胞瘤细胞系( U251、T98G和 SHG44)及 HA1800细胞中 miR-568表达分别为( 1.01±0.09)、(0.39±0.03)、(0.58±0.05)及( 0.46±0.04)AKR1B10 mRNA表达分别为( 0.98±0.08)、(2.45±0.2)、(2.16±0.21)及( 2.37±0.23)， AKR1B10蛋白表达分别为( 0.12±0.03)、，(0.61±0.05)、(0.51±0.04)及( 0.59±0.05)胶质母细胞瘤细胞系( U251、T98G和 SHG44)中 miR-568表达低于 HA1800细胞( P< 0.05)， AKR1B10 mRNA和蛋白表达高于，HA1800细胞( P<0.05)。上调 miR-568或下调 AKR1B10后， U251细胞增殖活性［(0.61±0.06)、(0.69±0.06)］、CyclinD1［(0.32±0.03)、(0.35±0.03)］和 Bcl-2蛋白表达［(0.29±0.03)、(0.32±0.03)］降低( P<0.05)， U251细胞凋亡率［( 22.41±2.15)%、(21.26±2.14)%］、 p21［(0.58±0.05)、(0.56±0.05)］和 Bax蛋白表达［(0.72±0.07)、(0.67± |
| 英文摘要: |
| Objective To investigate the effect and mechanism of microRNA-568 (miR-568) on the proliferation and apoptosis of glioblastoma cells.Methods Cultured normal HA1800 astrocytes and glioblastoma cell lines (U251, T98G and SHG44) were pur chased from Shanghai Cell Bank, Chinese Academy of Sciences. The mRNA expression of miR-568 and aldosterone reductase family 1 member B10 (AKR1B10) was detected by qRT-PCR, and the protein expression of AKR1B10 was detected by Western blotting. Taking U251 cells as the research objects, U251 cells with upregulated miR-568 or downregulated AKR1B10 were constructed. MTT, flow cy tometry and Western blotting assays were used to detect cell proliferation, apoptosis and the expression of CyclinD1, p21, Bcl-2 and Bax proteins in cells. The dual-luciferase reporter gene experiment verified the regulatory relationship between miR-568 and AKR1B10.Results The expression of miR-568 in glioblastoma cell lines (U251, T98G and SHG44) and HA1800 cells was (1.01±0.09), (0.39±0.03), (0.58±0.05) and (0.46±0.04), respectively. The expression of AKR1B10 mRNA was (0.98±0.08), (2.45±0.2), (2.16±0.21) and (2.37±0.23), respectively, and the AKR1B10 protein expression was (0.12±0.03), (0.61±0.05), (0.51±0.04) and (0.59±0.05),respectively. The expression of miR-568 in glioblastoma cell lines (U251, T98G and SHG44) was lower than that in HA1800 cells (P <0.05), and the mRNA and protein expression levels of AKR1B10 were higher than those in HA1800 cells (P < 0.05). After upregulating miR-568 or downregulating AKR1B10, U251 cell proliferation activity [(0.61±0.06), (0.69±0.06)], CyclinD1 [(0.32±0.03), (0.35±0.03)]and Bcl-2 protein expression [(0.29±0.03), (0.32±0.03)] decreased (P < 0.05), U251 cell apoptosis rate [(22.41±2.15)% , (21.26±2.14)%], p21 [(0.58±0.05), (0.56±0.05)] and Bax protein expression [(0.72±0.07), (0.67±0.07)] increased (P < 0.05). miR-568 targets and negatively regulates AKR1B10. Upregulation of AKR1B10 reverses the effects of upregulation of miR-568 on U251 cell prolifera tion and apoptosis.Conclusion Upregulation of miR-568 inhibits glioblastoma cell proliferation and promotes apoptosis by targeting and negatively regulating AKR1B10. |
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