解剖学报

解剖学报 ›› 2024, Vol. 55 ›› Issue (5): 573-581.doi: 10.16098/j.issn.0529-1356.2024.05.008

• 肿瘤生物学 • 上一篇    下一篇

非染色体结构维护凝集素Ⅰ复合物亚基G通过Akt信号通路促进卵巢癌细胞的增殖、迁移和侵袭

张明姝1,3 王艺慧1  张晴1  叶丽平1,2*
  

  1. 1.锦州医科大学基础医学院病理生理学教研室，辽宁 锦州  121001; 2.锦州医科大学生物人类学研究所，辽宁 锦州  121001; 3.沈阳市第五人民医院医学检验中心，沈阳  110000
  • 收稿日期:2023-08-26 修回日期:2023-12-28 出版日期:2024-10-06 发布日期:2024-10-06
  • 通讯作者: 叶丽平 E-mail:yeliping@jzmu.edu.cn
  • 基金资助:
    辽宁省科技厅自然基金资助计划

Non-structural maintenance of chromosome condensin Ⅰ complex subunit G promoting the proliferation, migration and invasion of ovarian cancer cells by the Akt signaling pathway

ZHANG  Ming-shu1,3  WANG  Yi-hui1  ZHANG  Qing1  YE  Li-ping1,2*    

  1. 1.Department of Pathophysiology, School of Basic Medical Sciences, Jinzhou Medical University, Liaoning Jinzhou 121001, China; 2.Institute of Biological Anthropology, Jinzhou Medical University, Liaoning Jinzhou 121001, China; 3.Medical Laboratory Center of Shenyang Fifth People’s Hospital, Shenyang 110000, China
  • Received:2023-08-26 Revised:2023-12-28 Online:2024-10-06 Published:2024-10-06
  • Contact: YE Li-ping E-mail:yeliping@jzmu.edu.cn

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摘要：

目的   探讨非染色体结构维护凝集素Ⅰ复合物亚基G（NCAPG）调控卵巢癌细胞的增殖、迁移和侵袭的机制。 方法   生物信息学GEPIA数据库分析NCAPG在卵巢癌组织中的差异表达。Western blotting检测正常卵巢上皮细胞IOSE80、卵巢癌A2780和SKOV3细胞中NCAPG的蛋白表达。NCAPG siRNA沉默实验分为空白组、对照组、siNCAPG-1组和siNCAPG-2组。NCAPG过表达实验分为空白组、对照、NCAPG组、NCAPG+MK2206组和MK2206组。MTT实验检测细胞增殖活性；细胞划痕实验和Transwell实验评估细胞的迁移和侵袭能力；Western blotting检测细胞的磷酸化Akt（p-Akt）、总Akt（t-Akt）、增殖细胞核抗原（PCNA）、基质金属蛋白酶9（MMP-9）、波形蛋白（vimentin）、N-钙黏蛋白（N-cadherin）和E-钙黏蛋白（E-cadherin）的表达水平。 结果   NCAPG在卵巢癌组织和卵巢癌细胞中高表达。沉默NCAPG可明显抑制卵巢癌SKOV3细胞的增殖、迁移和侵袭，Akt、PCNA、MMP-9、vimentin和N-cadherin表达减少，E-cadherin表达增多。过表达NCAPG质粒可促进卵巢癌A2780细胞增殖、迁移和侵袭，p-Akt、PCNA、MMP-9、vimentin和N-cadherin表达增多，E-cadherin表达降低。Akt抑制剂MK2206可明显抑制NCAPG的上述作用。 结论   NCAPG激活Akt信号通路，调控PCNA、MMP-9和上皮细胞-间充质转化（EMT）相关蛋白的表达，促进卵巢癌细胞的增殖、迁移和侵袭。 

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Abstract:

Objective   To explore the regulatory mechanism of non-structural maintenance of chromosome condensin I complex submit G (NCAPG) on proliferation, migration, and invasion of ovarian cancer cells.  Methods   The bioinformatics database was used to analyze the differential expression of NCAPG in ovarian cancer tissues. Western blotting was used to detect the protein expression of NCAPG in normal ovarian epithelial cells IOSE80, ovarian cancer A2780 and SKOV3 cells. The silencing experiments of NCAPG siRNA were divided into blank, control, siNCAPG-1 and siNCAPG-2 groups. The overexpression experiments of NCAPG plasmid were divided into blank, control, NCAPG, NCAPG+MK2206 and MK2206 groups. MTT assay was used to detect cell proliferation activity. Cell scoring assay and transwell assay were used to analyze cell migration and invasion. The protein expressions of p-Akt, total(t)-Akt, proliferative cellular nucleus antigen (PCNA), matrix metallopeptidase 9 (MMP-9), vimentin, N-cadherin, and E-cadherin were detected by Western blotting.  Results   NCAPG was highly expressed in ovarian cancer tissues and cells. Knockdown of NCAPG significantly inhibited the proliferation, invasion and migration of ovarian cancer SKOV3 cells. The protein expressions of p-Akt, PCNA, MMP-9, vimentin and N-cadherin decreased while E-cadherin expression increased. Overexpression of NCAPG significantly promoted the proliferation, invasion and migration of ovarian cancer A2780 cells. The protein expressions of pAkt, PCNA, MMP-9, vimentin, and N-cadherin increased while E-cadherin expression decreased. Akt inhibitor MK2206 significantly attenuated the above effects of NCAPG.  Conclusion  NCAPG promotes the proliferation, invasion, and migration of ovarian cancer cells by activating the Akt signaling pathway and regulating the expression of PCNA, MMP-9, and epithelial-mesenchymal transition (EMT)-related proteins. 

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