Glioma-associated oncogene homologue 2 promotes epithelial-mesenchymal transition in colon cancer cell line SW620

康清杰; 向　征

doi:10.19401/j.cnki.1007-3639.2020.04.003

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Glioma-associated oncogene homologue 2 promotes epithelial-mesenchymal transition in colon cancer cell line SW620

更新时间：2026-01-27

- Glioma-associated oncogene homologue 2 promotes epithelial-mesenchymal transition in colon cancer cell line SW620
- China Oncology Vol. 30, Issue 4, Pages: 254-260(2020)
- 作者机构：
  
  重庆医科大学附属第一医院胃肠外科,重庆,400016
- 作者简介：
- 基金信息：
- DOI：10.19401/j.cnki.1007-3639.2020.04.003
  CLC： R735.35
- Published Online：11 May 2020，
  
  Published：11 May 2020
- 稿件说明：
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康清杰, 向　征. 胶质瘤相关癌基因同源蛋白2促进结肠癌细胞系SW620的上皮-间质转化[J]. 中国癌症杂志, 2020, 30(4): 254-260.

康清杰, 向　征. Glioma-associated oncogene homologue 2 promotes epithelial-mesenchymal transition in colon cancer cell line SW620[J]. China Oncology, 2020, 30(4): 254-260.
康清杰, 向　征. 胶质瘤相关癌基因同源蛋白2促进结肠癌细胞系SW620的上皮-间质转化[J]. 中国癌症杂志, 2020, 30(4): 254-260. DOI： 10.19401/j.cnki.1007-3639.2020.04.003.

康清杰, 向　征. Glioma-associated oncogene homologue 2 promotes epithelial-mesenchymal transition in colon cancer cell line SW620[J]. China Oncology, 2020, 30(4): 254-260. DOI： 10.19401/j.cnki.1007-3639.2020.04.003.

摘要

背景与目的：胶质瘤相关癌基因同源蛋白2（glioma-associated oncogene homologue 2，GLI2）是Hedgehog信号通路重要的转录因子，不仅参与正常的细胞分化，而且在多种肿瘤细胞中异常激活，与肿瘤转移密切相关。探讨GLI2与结肠癌细胞系SW620上皮-间质转化（epithelial-mesenchymal transition，EMT）的关系及其可能机制。方法：采用实时荧光定量聚合酶链反应（real-time fluorescence quantitative polymerase chain reaction，RTFQ-PCR）检测人结肠癌细胞系SW620、SW480、HCT116和HT29中E-cadherin mRNA表达，以GLI2干扰慢病毒感染SW620细胞，用RTFQ-PCR和蛋白质印迹法（Western blot）检测细胞中GLI2 mRNA表达和蛋白水平，采用Transwell小室检测细胞侵袭、迁移能力，黏附实验检测同、异种细胞间黏附能力，Western blot检测细胞中p-AKT、N-cadherin、vimentin、MMP2和E-cadherin蛋白水平。结果：4种细胞系中，SW620的E-cadherin mRNA表达最低（P0.05），SW620转染72 h后，可见明显的荧光表达；与空病毒组和对照组相比，干扰组细胞的GLI2表达降低（P0.05）；细胞侵袭和迁移能力减弱（P0.05）；同种细胞黏附能力增强（P0.05）；异种细胞黏附能力减弱（P0.05）；p-AKT、N-cadherin、vimentin和MMP-2的表达降低（P0.05）、E-cadherin表达增加（P0.05）。结论：GLI2可能通过上调p-AKT、N-cadherin、vimentin和MMP-2表达和抑制E-cadherin表达来促进结肠癌细胞系SW620的EMT。

Abstract

Background and purpose: Glioma-associated oncogene homologue 2 (GLI2) is an important transcription factor of Hedgehog signaling pathway

which is involved in not only normal cell differentiation

but also abnormal activation in a variety of tumor cells. GLI2 is closely related to tumor metastasis. This study aimed to explore the relationship between GLI2 and epithelial- mesenchymal transition (EMT) of colon cancer cell line SW620 and its possible mechanism. Methods: The expression of E-cadherin mRNA was confirmed by real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) in human colon cancer cell lines SW620

SW480

HCT116 and HT29. The SW620 cells were infected with GLI2 interference lentivirus. The expressions of GLI2 mRNA and protein were confirmed by RTFQ-PCR and Western blot. Transwell chamber was used to detect the ability of invasion and migration. Adhesion experiment was used to detect the ability of homogeneous and heterogeneous cell intercellular adhesion. Western blot was used to detect the protein expressions of p-AKT

N-cadherin

vimentin

MMP2 and E-cadherin. Results: The E-cadherin mRNA expression was the lowest in SW620 cell line among the 4 cell lines (P0.05). After SW620 cells were infected with GLI2 interference lentivirus for 72 h

significant fluorescence expression could be seen. Compared with the empty vector group and the control group

the expression of GLI2 was lower (P0.05)

the invasion and migration abilities were diminished (P0.05)

the homogeneous cell intercellular adhesion ability increased (P0.05)

the heterogeneous cell intercellular adhesion ability decreased (P0.05)

the protein expressions of p-AKT

N-cadherin

vimentin and MMP-2 decreased (P0.05)

and the protein expression of E-cadherin increased in the interference group (P0.05). Conclusion: GLI2 may promote EMT of colon cancer cell line SW620 by upregulating the expressions of p-AKT

N-cadherin

vimentin and MMP-2 and inhibiting the expression of E-cadherin.

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