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

目的探究抑制IL-17A的表达对脓毒血症小鼠急性肾脏损伤的影响。 方法24只小鼠按照随机数字表法均分为对照组、模型组和抑制剂组。模型组和抑制剂组小鼠腹腔注射高剂量LPS(10 mg/kg)建立脓毒血症急性肾损伤模型,抑制剂组给与IL-17A抑制剂SGC-CBP30(30 mg/kg)。检测血清肌酐、尿素氮和炎症因子水平,分析肾功能的变化,通过HE染色和过碘酸雪夫染色分析肾脏病理变化,分析肾脏炎症因子水平和细胞凋亡蛋白的变化。 结果IL-17A抑制剂处理能够显著下调脓毒血症小鼠血清肌酐、尿素氮和炎症因子IL-6和TNF-α水平(P＜0.05)；抑制IL-17A的表达能够显著改善脓毒血症小鼠肾脏的损伤,下调肾脏炎症因子和细胞凋亡蛋白的表达。 结论抑制IL-17A的表达能够改善脓毒血症小鼠急性肾损伤。

Effects of miR-363-5p targeting TRIM14 on chemotherapy-induced apoptosis in breast cancer cell lines

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.