China Oncology ›› 2020, Vol. 30 ›› Issue (4): 254-260.doi: 10.19401/j.cnki.1007-3639.2020.04.003

• Article • Previous Articles     Next Articles

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

KANG Qingjie, XIANG Zheng   

  1. Department of Gastrointestinal Surgery, First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
  • Online:2020-04-30 Published:2020-05-11
  • Contact: XIANG Zheng E-mail: xiangzhengly@163.com

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 (P<0.05). 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 (P<0.05), the invasion and migration abilities were diminished (P<0.05), the homogeneous cell intercellular adhesion ability increased (P<0.05), the heterogeneous cell intercellular adhesion
ability decreased (P<0.05), the protein expressions of p-AKT, N-cadherin, vimentin and MMP-2 decreased (P<0.05), and the protein
expression of E-cadherin increased in the interference group (P<0.05). 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.

Key words: Glioma-associated oncogene homologue 2, SW620, Epithelial-mesenchymal transition, Metastasis