解剖学报

解剖学报 ›› 2022, Vol. 53 ›› Issue (2): 196-202.doi: 10.16098/j.issn.0529-1356.2022.02.009

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MEX3A通过PI3K/Akt信号通路促进结直肠癌细胞的增殖和迁移

闫婷1,2 赵继凯3 王恩华1*   

  1. 1.中国医科大学基础医学院病理学教研室，沈阳 110122; 2.北京战区总医院病理科，沈阳 110016; 3.北部战区总医院心血管外科，沈阳 110016
  • 收稿日期:2020-11-13 修回日期:2020-12-23 出版日期:2022-04-06 发布日期:2022-04-06
  • 通讯作者: 王恩华 E-mail:wangwh@hotmail.com
  • 基金资助:
    N-端RASSFs中7和10对肺癌细胞不同作用的分子机制

MEX3A promotes proliferation and migration of colorectal cancer cells via PI3K/Akt signaling pathway

YAN Ting1,2   ZHAO Ji-kai3  WANG En-hua1*   

  1. 1.Department of Pathology, College of Basic Medical Science of China Medical University, Shenyang 110122, China; 2.Department of Pathology, General Hospital of Northern Theater Command, Shenyang 110016, China; 3.Department of Cardiovascular Surgery, General Hospital of Northern Theater Command, Shenyang 110016, China
  • Received:2020-11-13 Revised:2020-12-23 Online:2022-04-06 Published:2022-04-06
  • Contact: WANG En-hua E-mail:wangwh@hotmail.com

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摘要：

目的 探讨MEX3A在结直肠癌（CRC）中的表达水平，及MEX3A对结直肠癌细胞增殖和迁移的影响及作用机制。  方法 通过TCGA数据库获取327例数据（正常组织41例，肿瘤组织286例），收集临床样本104例（癌旁组织27例，癌组织77例），进行免疫组织化学染色，分析MEX3A在结直肠癌和正常组织间表达的差异。利用Western blotting和免疫荧光染色检测结直肠癌细胞系中MEX3A的表达水平，选取CL187细胞作为后续研究载体。通过MEX3A小干扰RNA（siMEX3A）转染的方式抑制CL187细胞中MEX3A的表达，联合或单独使用PI3K/Akt通路激活剂740 Y-P，采用MTT、集落形成实验和Transwell实验测定下调MEX3A后CL187细胞的增殖和迁移，并通过Western blotting检测其PI3K、p-PI3K、Akt和p-Akt的表达水平。  结果 TCGA数据库、免疫组织化学染色、Western blotting结果显示，MEX3A在结直肠癌中高表达，免疫荧光染色提示，MEX3A富集于细胞质与细胞核中；在MTT、集落形成实验和Transwell实验中，siMEX3A组CL187细胞的增殖和迁移能力显著低于对照组（P<0.05）；Western blotting结果显示，siMEX3A组的p-PI3K和p-Akt的表达水平显著下调（P<0.05），而当加入740 Y-P激活PI3K/Akt信号通路后，siMEX3A对CL187细胞的增殖和迁移能力抑制作用被部分逆转。  结论 MEX3A在结直肠癌中高表达，并通过PI3K/Akt信号通路促进结直肠癌细胞的增殖和迁移。

关键词: MEX3A, 基因沉默, 结直肠癌, 细胞增殖, 细胞迁移, 磷脂酰肌醇-3激酶/蛋白激酶B信号通路, 免疫组织化学, 人

Abstract:

Objective To investigate the expression of MEX3A in colorectal cancer (CRC), and to explore the effect and mechanism of MEX3A on the proliferation and migration of colorectal cancer cells.   Methods Totally 327 cases of data(41 normal tissues and 286 tumor tissues) were obtained from TCGA database, and 104 cases of clinical samples(77 cases tissues and 27 paracancerous tissues) were collected for immunohistochemistry, then analysed the differences in MEX3A expression between CRC tissues and normal tissues. Western blotting and immunofluorescence staining were used to evaluate the differential expression of MEX3A in CRC cell lines.  CL187 cells were selected as the follow-up research vector. Small interfering RNA of MEX3A(siMEX3A) was transfected into CL187 cells to inhibit the expression of MEX3A. The proliferation and migration of CL187 cells were measured by MTT, colony formation assay and Transwell assay. The expression of PI3K, p-PI3K, Akt and p-Akt were detected by Western blotting.   Results TCGA database, immunohistochemistry and Western blotting analysis showed that MEX3A was highly expressed in colorectal cancer. The result  of immunofluorescence staining showed that MEX3A was concentrated in the cytoplasm and the nucleus. In MTT, colony formation assay and Transwell assay, the proliferation and migration ability of CL187 cells in siMEX3A group decreased significantly than those in control group (P<0.05). Western blotting result  showed that the expression of p-PI3K and p-Akt in siMEX3A group down-regulated significantly (P<0.05), and the inhibition of proliferation and migration ability of CL187 cells induced by siMEX3A group could be reversed by 740 Y-P via activating the PI3K/Akt signaling pathway.   Conclusion MEX3A is highly expressed in colorectal cancer and promotes the proliferation and migration of CRC cells via PI3K/Akt signaling pathway.

Key words: MEX3A, Gene sliencing, Colorectal cancer, Cell proliferation, Cell migration, Phosphatidylinositol 3-kinase/protein kinase B signaling pathway, Immunohistochemistry, Human

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