基础医学与临床 ›› 2025, Vol. 45 ›› Issue (11): 1473-1479.doi: 10.16352/j.issn.1001-6325.2025.11.1473

• 研究论文 • 上一篇    下一篇

miR-1287- 5p上调促进人食管癌细胞系KYSE30对紫杉醇的耐药

王居正1, 卢佳煜2, 王擎实1, 刘雯2, 包博2, 李一鸣2, 卢强3*   

  1. 1.咸阳市第一人民医院 胸外科,陕西 咸阳 712000;
    2.空军军医大学 基础医学院,陕西 西安 710032;
    3.空军军医大学唐都医院 胸外科, 陕西 西安 710038
  • 收稿日期:2024-10-24 修回日期:2025-01-08 出版日期:2025-11-05 发布日期:2025-10-24
  • 通讯作者: *luqiang0103o@163.com

Upregulation of miR-1287-5p promotes paclitaxel resistance in human esophageal cancer cell line KYSE30

WANG Juzheng1, LU Jiayu2, WANG Qingshi1, LIU Wen2, BAO Bo2, LI Yiming2, LU Qiang3*   

  1. 1. Department of Thoracic Surgery, Xianyang First People's Hospital, Xianyang 712000;
    2. College of Basic Medicine, Air Force Medical University, Xi'an 710032;
    3. Department of Thoracic Surgery, Tangdu Hospital, Air Force Medical University, Xi'an 710038, China
  • Received:2024-10-24 Revised:2025-01-08 Online:2025-11-05 Published:2025-10-24
  • Contact: *luqiang0103o@163.com

摘要: 目的 分析 miR-1287-5p 影响人食管癌细胞系KYSE30对紫杉醇敏感性的机制。方法 KYSE30细胞分为对照组、转染miR-1287-5p mimic和inhibitor组,使用RT-qPCR验证转染率。CCK-8法检测细胞活力和半数抑制浓度(IC50)。划痕实验、Transwell小室法和TUNEL法分别评估细胞的迁移、侵袭能力和凋亡率。Western blot和免疫细胞化学(ICC)检测细胞中Akt和GSK-3β蛋白的表达及其定位。结果 RT-qPCR结果显示,miR-1287-5p mimic组的miR-1287-5p表达明显高于miR-NC组和对照组(P<0.05),而miR-1287-5p inhibitor组的表达水平明显低于miR-NC组和对照组(P<0.05)。miR-1287-5p mimic组的细胞存活率高于miR-NC组及miR-1287-5p inhibitor组(P<0.05);miR-1287-5p mimic组的细胞迁移率、侵袭细胞数目较miR-NC组高(P<0.05),凋亡率相较于miR-NC组降低(P<0.05);而miR-1287-5p inhibitor组的细胞迁移率、侵袭细胞数目较miR-NC组降低/减少(P<0.05),凋亡率相较于miR-NC组升高(P<0.05);miR-1287-5p mimic组Akt和GSK-3β的表达水平显著高于miR-NC组(P<0.05),而miR-1287-5p inhibitor组的表达水平显著低于miR-NC组(P<0.05)。结论 上调miR-1287-5p可促进食管癌细胞系的迁移和侵袭能力,抑制细胞凋亡,促进对紫杉醇耐药性。

关键词: miR-1287-5p, 食管癌, 紫杉醇耐药

Abstract: Objective To discover the mechanism by which miR-1287-5p affects the sensitivity of human esophageal cancer cell line KYSE30 to paclitaxel. Methods KYSE30 cells were divided into control group, group of transfected with miR-1287-5p mimic and inhibitor groups. RT-qPCR was used to detect the transfection rate. A paclitaxel-resistant cell line was established and cell viability and half inhibitory concentration (IC50) were detected by CCK-8 assay. The scratch test, Transwell chamber test and TUNEL method were used to evaluate the migration, invasion and apoptosis of cells . Western blot and immunocytochemistry (ICC) were used to detect the expression and localization of Akt and GSK-3β in cells. Results The expression level of miR-1287-5p in the miR-1287-5p mimic group was significantly higher than that in the miR-NC group and control group (P<0.05), while the expression level of the miR-1287-5p inhibitor group was significantly lower than that in miR-NC group and control group (P<0.05). The cell survival rate of the miR-1287-5p mimic group was higher than that of the miR-NC group and the miR-1287-5p inhibitor group (P<0.05). The cell migration rate and number of invasive cells in the miR-1287-5p mimic group were higher than those of the miR-NC group(P<0.05), and the apoptosis rate was lower than that of the miR-NC group (P<0.05). While in miR-1287-5p, the cell migration rate was lower and invasive cells were less in the inhibitor group and the apoptosis rate was increased as compared to the miR-NC group (P<0.05).The expression of Akt and GSK-3β in the miR-1287-5p mimic group was significantly increased than in the miR-NC group (P<0.05), while the expression in the miR-1287-5p inhibitor group was significantly inhibited than in miR-NC group (P<0.05). Conclusions Up-regulation of miR-1287-5p can promote the migration and invasion of paclitaxel-resistant cell lines, inhibit cell apoptosis and thereby promote the development of paclitaxel resistance.

Key words: miR-1287-5p, esophageal cancer, paclitaxel resistance

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