| 摘要: |
| ［摘要］ 目的 探讨miR-138-5p对乳腺癌细胞他莫昔芬（TAM）耐药性的影响及其机制。方法 体外培养乳腺癌细胞MCF-7和TAM耐药细胞株MCF-7/TAM，设置正常对照组（MCF-7细胞）、耐药对照组（MCF-7/TAM细胞）、LV-NC组（MCF-7/TAM细胞+慢病毒空载体）和LV-miR-138-5p mimics组（MCF-7/TAM细胞+miR-138-5p mimics慢病毒）。通过实时荧光定量PCR（qRT-PCR）法检测各组细胞miR-138-5p表达水平；通过MTT法检测各组细胞增殖抑制率；通过流式细胞术检测各组细胞凋亡率；通过MDC染色法检测各组细胞自噬小体数量；通过Western blot法检测各组细胞LC3Ⅱ、Beclin-1、Bcl-2蛋白表达水平。结果 与正常对照组相比较，耐药对照组、LV-NC组细胞miR-138-5p、增殖抑制率、凋亡率、Bcl-2蛋白表达水平均显著降低（P<0.05），蛋白LC3Ⅱ、Beclin-1表达水平及自噬小体数显著升高（P<0.05）。过表达miR-138-5p后，细胞增殖抑制率、凋亡率、蛋白Bcl-2表达水平显著升高（P<0.05），蛋白LC3Ⅱ、Beclin-1表达水平及自噬小体数显著降低（P<0.05）。结论 上调miR-138-5p可能通过抑制自噬，降低乳腺癌细胞他莫昔芬耐药性。 |
| 关键词: miR-138-5p 乳腺癌细胞 他莫昔芬 耐药性 细胞自噬 |
| DOI：10.3969/j.issn.1674-3806.2023.09.09 |
| 分类号:R 737.9 |
| 基金项目:2019年青海省卫生健康科研课题（编号：2019-wjzdx-65） |
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| A study of the effect of miR-138-5p on the resistance of breast cancer cells to tamoxifen by regulating autophagy in vitro |
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YAO Hao-ming, LI Ying
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Department of Pharmacy, Qinghai Red Cross Hospital, Xining 810000, China
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| Abstract: |
| ［Abstract］ Objective To study the effect of miR-138-5p on the resistance of breast cancer cells to tamoxifen(TAM) and its mechanism. Methods Breast cancer cells MCF-7 and TAM resistant cell line MCF-7/TAM were cultured in vitro. Normal control group(MCF-7 cells), drug-resistant control group(MCF-7/TAM cells), LV-NC group(MCF-7/TAM cells+lentivirus empty vector) and LV-miR-138-5p mimics group(MCF-7/TAM cells+miR-138-5p mimics lentivirus) were set up. The expression level of miR-138-5p in each group was detected by quantitative real-time polymerase chain reaction(PCR)(qRT-PCR). The inhibition rate of cell proliferation in each group was detected by methyl thiazolyl tetrazolium(MTT) assay. The apoptosis rate in each group was detected by flow cytometry. The number of autophagosomes in each group was detected by monodansylcadaverine(MDC) staining. The protein expression levels of LC3Ⅱ, Beclin-1 and Bcl-2 in each group were detected by Western blot. Results Compared with those in the normal control group, the expression levels of miR-138-5p, proliferation inhibition rate, apoptosis rate and Bcl-2 protein in the drug-resistant control group and the LV-NC group were significantly decreased(P<0.05), while the expression levels of protein LC3Ⅱ and Beclin-1 and the number of autophages were significantly increased(P<0.05). After overexpression of miR-138-5p, cell proliferation inhibition rate, apoptosis rate and protein Bcl-2 expression were significantly increased(P<0.05), while the expression levels of protein LC3Ⅱ and Beclin-1 and the number of autophagosomes were significantly decreased(P<0.05). Conclusion Up-regulation of miR-138-5p may decrease the resistance of breast cancer cells to tamoxifen by inhibiting autophagy. |
| Key words: miR-138-5p Breast cancer cells Tamoxifen(TAM) Drug resistance Autophagy |
