Background and purpose: Glioma-associated oncogene homolog 2 (Gli2) is an important transcription factor of Hedgehog signaling pathway

which is closely related to not only the growth of normal cells

but also abnormal activation in a variety of tumor cells. This study aimed to explore the effect of Gli2 on the proliferation and apoptosis of colon cancer cell line SW620 and its possible mechanism. Methods: The SW620

cells were infected with Gli2 interference lentivirus. The expressions of Gli2 mRNA and protein were confirmed by real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) and Western blot. Cell proliferation was detected by cell counting kit-8 (CCK-8) assay

colony formation assay and doubling time. Flow cytometry was used to detect the cell cycle and apoptosis of SW620. Western blot was used to detect the protein expressions of ERK1/2

p-ERK1/2

Bcl-2

Bax and cyclin D1. Results: After infection of SW620 with Gli2 interference lentivirus for 72 h

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

the expression of Gli2 in interference group was effectively inhibited (P0.05); cell proliferation was significantly reduced (P0.05); the cell cycle was arrested

and G

1

phase cell proportion was increased (P0.05); the apoptotic rate was significantly increased (P0.05); the protein expressions of ERK1/2

p-ERK1/2

Bcl-2 and cyclin D1 were decreased (P0.05)

and the expression of Bax was increased (P0.05). Conclusion: The siRNA-mediated Gli2 silencing significantly inhibited the proliferation of colon cancer cell line SW620 and promoted apoptosis

which may be related to the down-regulation of p-ERK1/2

Bcl-2 and cyclin D1 expressions and up-regulation of Bax expression.