首页 | 本学科首页   官方微博 | 高级检索  
     

miR-502-3p 通过靶向结合 CBL 抑制卵巢癌增殖并诱导凋亡
引用本文:张玲艳,王海红,刘晶晶. miR-502-3p 通过靶向结合 CBL 抑制卵巢癌增殖并诱导凋亡[J]. 医学分子生物学杂志, 2022, 19(3): 181-186. DOI: 10.3870/j.issn.1672-8009.2022.03.001
作者姓名:张玲艳  王海红  刘晶晶
作者单位:1盐城市滨海县人民医院妇产科 江苏省盐城市, 224500 2北京市朝阳医院内科 北京市, 100029
摘    要:
目的 探究微小 RNA 502-3p (micro RNA 502-3p, miR-502-3p) 通过靶向结合 Casitas B 细胞淋巴瘤 (Casitas B-cell lymphoma, CBL) 参与卵巢癌增殖和凋亡的机制。 方法 下载 GSE66957、 GSE119056、TCGA_ OV 卵巢癌相关数据矩阵, 分析 miR-502-3p、 CBL 与卵巢癌的关系; 构建过表达 miR-502-3p、 CBL的 SKOV3 和 HO8910 细胞系, 分别采用细胞计数试剂盒 ( cell counting kit 8, CCK-8)、 克隆形成实验、 流式细胞术检测细胞增殖和凋亡情况; 通过荷瘤裸鼠实验, 观察过表达 CBL 对肿瘤生长的影响; 验证 miR502-3p 与 CBL 的靶向关系。 结果 生物信息学分析显示, 卵巢癌组织中 CBL 水平高于癌旁组织, miR-502-3p 水平低于癌旁组织, CBL 水平与患者预后、 细胞增殖基因表达有关 (P< 0. 05)。 miR-502-3p 与 CBL 存在靶向关系, 与 Vector 组比较, CBL 组肿瘤的体积及重量增加 (P< 0. 05); 与 miR-NC 组比较, miR-502-3p组 SKOV3、 HO8910 细胞中 CBL 蛋白表达、 细胞活力、 克隆数降低, 细胞凋亡率升高 (P< 0. 05), 但 CBL可逆转上述细胞变化。 结论 miR-502-3p 可通过靶向下调 CBL 抑制卵巢癌细胞的增殖, 并诱导其凋亡。

关 键 词:卵巢癌   miR-502-3p   Casitas B 细胞淋巴瘤   细胞增殖   细胞凋亡  

miR-502-3 p Inhibit Proliferation and Induce Apoptosis in Ovarian Cancer by Targeting CBL
ZHANG Lingyan,WANG Haihong,LIU Jingjing. miR-502-3 p Inhibit Proliferation and Induce Apoptosis in Ovarian Cancer by Targeting CBL[J]. Journal of Medical Molecular Biology, 2022, 19(3): 181-186. DOI: 10.3870/j.issn.1672-8009.2022.03.001
Authors:ZHANG Lingyan  WANG Haihong  LIU Jingjing
Affiliation:1Department of Obstetrics and Gynecology, Binhai County People’s Hospital, Yancheng, Jiangsu,224500, China 2Department of Internal Medicine, Beijing Chaoyang Hospital, Beijing, 100029, China
Abstract:
Objective To explore the effects of micro RNA 502-3p (miR-502-3p) on the proliferation and apoptosis of ovarian cancer cells by targeting Casitas B-cell lymphoma ( CBL). Methods The ovarian cancer related datasets GSE66957, GSE119056 and TCGA _ OV weredownloaded and the relationship between ovarian cancer and miR-502-3p or CBL was analyzed. TheSKOV3 and HO8910 cell lines with overexpressed miR-502-3p or/ and CBL were constructed. Thecell proliferation and apoptosis were detected by cell counting kit 8 (CCK-8), clone formation assay and flow cytometry. The effect of CBL overexpression on tumor growth was observed in tumor bearing nude mice. The targeting relationship between miR-502-3p and CBL was verified. Results Bioinformatics analysis showed that the expression level of CBL in ovarian cancer tissues was higherthan that in para-cancerous tissues, while the expression level of miR-502-3p was lower in cancertissues than in para-cancerous tissues (P < 0. 05). The expression level of CBL was related to theprognosis of ovarian cancer and the expression of cell proliferation-related genes (P < 0. 05). Therewas a targeting relationship between miR-502-3p and CBL. The volume and weight of tumors weresignificantly increased in the CBL group compared with the vector group (P< 0. 05). The expressionlevel of CBL protein, cell viability and number of clones formed in SKOV3 and HO8910 cell lineswere significantly decreased and the apoptosis rate was significantly increased in the miR-502-3pgroup compared with the miR-NC group (P < 0. 05). However, CBL overexpression could reversethe above changes. Conclusion miR-502-3p can inhibit the proliferation and induce the apoptosisof ovarian cancer cells by down-regulating CBL.
Keywords:ovarian cancer   miR-502-3p   Casitas B-cell lymphoma   cell proliferation   apoptosis  
本文献已被 万方数据 等数据库收录!
点击此处可从《医学分子生物学杂志》浏览原始摘要信息
点击此处可从《医学分子生物学杂志》下载免费的PDF全文
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号