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.