| 邹学红,汪俊,王芳,等.微小 RNA-338-3p靶向调控高迁移率族蛋白 B1增强子宫内膜癌对紫杉醇敏感性的研究[J].安徽医药,2021,25(8):1613-1618. |
| 微小 RNA-338-3p靶向调控高迁移率族蛋白 B1增强子宫内膜癌对紫杉醇敏感性的研究 |
| MiR-338-3p enhances the sensitivity of endometrial carcinoma to paclitaxel by targeting HMGB1 |
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| DOI：10.3969/j.issn.1009-6469.2021.08.033 |
| 中文关键词: 子宫内膜肿瘤 miR-338-3p 高迁移率族蛋白 B1 紫杉醇 |
| 英文关键词: Endometrial neoplasms miR-338-3p High-mobilitygroupboxprotein-1 Paclitaxel |
| 基金项目:河南省科技攻关项目( 182102310153) |
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| 中文摘要: |
| 目的探讨 miR-338-3p靶向调控高迁移率族蛋白 B1(HMGB1)影响子宫内膜癌对紫杉醇(Paclitaxel，PTX)敏感性的分子机制。方法实时荧光定量聚合酶链反应( qRT-PCR)和蛋白印迹法( Western blottingting)检测 miR-338-3p和 HMGB1在子宫内膜癌细胞 Ishikawa和 HEC-1B中的表达；双荧光素酶报告基因实验验证 miR-338-3p和 HMGB1之间的靶向关系；将 Ishikawa和 HEC-1B细胞分为如下 5组: miR-338-3p组(转染 miR-338-3p mimics组)、 miR-NC组(转染 miRNA阴性对照组)、 si-HMGB1组(转染干扰 RNA)、 si-NC组(转染 siRNA阴性对照)、 miR-338-3p+HMGB1组(共转染 miR-338-3pmimics和 pcDNA3.0 HMGB1组)。将各组用转染试剂转染至细胞，用不同浓度的 PTX处理上述转染组细胞， CCK-8法检测 Ishikawa和 HEC-1B细胞增殖， Annexin V-FITC/PI检测细胞凋亡， Western blotting检测 HMGBI蛋白表达。结果与人正常子宫内膜上皮细胞 ESC相比， miR338-3p在子宫内膜癌细胞 Ishikawa和 HEC-1B中表达下调［(1.00±0.10)比( 0.51±0.04)、(0.46±0.04)］而 HMGB1则相反； miR338-3p靶向并负性调节 HMGB1表达；过表达 miR-338-3p抑制子宫内膜癌细胞 Ishikawa和 HEC-1B增殖，，促进凋亡，增加其对 PTX敏感，与敲低 HMGB1结果一致； HMGB1可部分逆转 miR-338-3p对子宫内膜癌细胞增殖，凋亡以及对 PTX敏感性的影响。结论 miR-338-3p通过负性调控 HMGB1抑制子宫内膜癌细胞 Ishikawa和 HEC-1B增殖，促进凋亡和增强其对 PTX敏感性。 |
| 英文摘要: |
| Objective To investigate the molecular mechanism of the effect of miR-338-3p on the sensitivity of endometrial carcinoma to paclitaxel (PTX) by targeting HMGB1.Methods The expression of miR-338-3p and HMGB1 in endometrial carcinoma cells Ishikawa and HEC-1B was detected by RT-qPCR and western blotting. The dual luciferase reporter gene assay was performed to confirm the relationship between miR-338-3p and HMGB1. Ishikawa and HEC-1B cells were divided into the following five groups: miR338-3p group (transfected with miR-338-3p mimics group), miR-NC group (transfected with miR-NC group), si-HMGB1 group (transfected with interfering RNA), si-NC group (transfected with siRNA negative control group), miR-338-3p+HMGB1 group (co-transfected with miR-338-3p mimics and pcDNA3.0 HMGB1 group). The cells were treated with different concentrations of PTX. CCK-8 was used to detect the proliferation of Ishikawa and HEC-1B cells. Annexin V-FITC/PI was conducted to detect apoptosis. The expression of HMGBI protein was detected by western blotting.Results miR-338-3p expression was down-regulated, while HMGB1 was upregulated in endometrial carcinoma cells Ishikawa and HEC-1B[(1.00±0.10) vs. (0.51±0.04),(0.46±0.04)]. miR-338-3p targeted and negatively regulated the expression of HMGB1. Overexpression of miR-338-3p inhibited the proliferation of Ishikawa and HEC-1B, promotedapoptosis and increased their sensitivity to PTX, which was consistent with knock down of HMGB1. HMGB1 can attenuated the effectof miR-338-3p on the proliferation, apoptosis and PTX sensitivity of endometrial carcinoma cells.Conclusion miR-338-3p can target HMGB1 to inhibit the proliferation of Ishikawa and HEC-1B cells, promote apoptosis and enhance their sensitivity to PTX. |
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