| 张军,吴淑宁,陈嘉丽,彭大伟,李杰,李杏,李鸽姿.miR-363-5p靶向TRIM14对化疗药物诱导的乳腺癌细胞系凋亡的影响.[J].中南医学科学杂志.,2022,(6):823-827. |
| miR-363-5p靶向TRIM14对化疗药物诱导的乳腺癌细胞系凋亡的影响 |
| Effects of miR-363-5p targeting TRIM14 on chemotherapy-induced apoptosis in breast cancer cell lines |
| 投稿时间：2021-12-27 修订日期：2022-05-15 |
| DOI：10.15972/j.cnki.43-1509/r.2022.06.010 |
| 中文关键词: miR-363-5p TRIM14 乳腺癌细胞系 凋亡 化疗药物 [ |
| 英文关键词:miR-363-5p TRIM14 breast cancer apoptosis chemotherapy |
| 基金项目:广东省医学科研基金(A2021161)；深圳市南山区科技局项目(南卫2018078) 作者简介:张军,副主任医师,研究方向为乳腺癌、甲状腺癌基础研究和临床诊治,E-mail为Zhangjunshekou2022@163.com。 |
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| 中文摘要: |
| 目的探讨miR-363-5p靶向三结构域蛋白14(TRIM14)对3种乳腺癌细胞系凋亡的影响。 方法采用实时荧光定量PCR法比较不同化疗药物诱导3种乳腺癌细胞(MCF-7、MDA-MB-435、MCF-12A)中miR-363-5p和TRIM14 mRNA表达水平,采用免疫组化法检测不同亚型乳腺癌组织TRIM14表达情况。采用Western blotting检测TRIM14蛋白表达。采用流式细胞术检测细胞凋亡情况。应用生物信息学方法预测miR-363-5p与TRIM14的结合位点,通过干扰miR-363-5p和TRIM14研究miR-363-5p对3种乳腺癌细胞中TRIM14的调控作用。Pearson相关分析各亚型乳腺癌组织中miR-363-5p与TRIM14的相关性。 结果3种化疗药物均能促进细胞凋亡,化疗药物处理3种亚型乳腺癌细胞后miR-363-5p表达上升,TRIM14 mRNA表达下降。荧光素酶报告基因实验发现TRIM14是miR-363-5p的靶基因。过表达miR-363-5p后,3种亚型乳腺癌细胞凋亡率上升,TRIM14蛋白和mRNA下降。敲低TRIM14后3种亚型乳腺癌细胞凋亡率上升,过表达TRIM14后3种亚型乳腺癌细胞凋亡率下降。3种亚型乳腺癌组织miR-363-5p与TRIM14表达呈负相关。 结论化疗药物诱导3种亚型乳腺癌细胞后miR-363-5p表达上升,miR-363-5p靶向抑制TRIM14表达,促进3种乳腺癌细胞系凋亡。 |
| 英文摘要: |
| To investigate the effect of miR-363-5p targeting triple domain protein 14 (TRIM14) on apoptosis of breast cancer cell lines. MethodsThe expression levels of miR-363-5p and TRIM14 mRNA in three breast cancer cells (MCF-7, MDA-MB-435, MCF-12A) induced by different chemotherapeutic drugs were compared by real-time fluorescent quantitative PCR, The expression of TRIM14 in different breast cancer tissues was detected by immunohistochemistry. The expression of TRIM14 protein was detected by western blotting. Cell apoptosis was detected by flow cytometry. Bioinformatics methods were used to predict the binding site of miR-363-5p and TRIM14, and to study the regulatory effect of miR-363-5p on TRIM14 in three breast cancer cells by interfering with miR-363-5p and TRIM14 mutation.Pearson correlation analysis of the correlation between miR-363-5p and TRIM14 in breast cancer tissues of various subtypes. ResultsAll three chemotherapeutic drugs promoted apoptosis. miR-363-5p expression increased and TRIM14 expression decreased after treatment of the three subtypes of breast cancer cells with chemotherapeutic drugs. The luciferase reporter gene assay junction identified TRIM14 as a direct target of miR-363-5p. After overexpression of miR-363-5p, apoptosis rate increased and TRIM14 protein and mRNA decreased in 3 subtypes of breast cancer cells. The apoptosis rate of the three subtypes of breast cancer cells increased after knockdown of TRIM14 and decreased after overexpression of TRIM14. miR-363-5p was negatively correlated with TRIM14 expression in the three subtypes of breast cancer tissues. ConclusionThe expression of miR-363-5p increased after the chemotherapeutic drug paclitaxel induced the three subtypes of breast cancer cells, and miR-363-5p promoted the apoptosis of three breast cancer cell lines by targeting the inhibition of TRIM14 expression. |
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