The aim of the present study was to investigate the role of
chemokine (C-X-C motif) ligand 8 (CXCL8) in the proliferation, invasiveness and
metastasis of
colon cancer and its role in the induction of epithelial-mesenchymal transition (EMT) via activation of the
phosphatidylinositol 3-kinase (PI3K)/
protein kinase B (Akt)/nuclear factor-κB (NF-κB) pathway. The plasmid vector containing CXCL8
cDNA was transfected into LoVo cells using Lipofectamine 2000
reagent. Real-time PCR and western blot analyses were performed to determine expression of CXCL8. MTT growth inhibition, scratch and Transwell invasion assays were conducted to assess cell proliferation, migration and invasiveness of the CXCL8-transfected LoVo cells. Western blot analyses were conducted to measure the levels of phosphorylation of
protein in the PI3K/Akt/NF-κB pathway in the CXCL8-transfected LoVo cells. Expression levels of CXCL8
mRNA and
protein were significantly increased in the CXCL8-transfected LoVo cells compared with levels in the control and empty-vector cells (P<0.05). Overexpression of CXCL8 increased proliferation of the LoVo cells and significant differences in cell viability were observed 48 h after transfection (P<0.05) and remained significant at 72 and 96 h. CXCL8-transfected LoVo cells had a significantly higher migration rate and doubled invasion. The CXCL8-transfected LoVo cells exhibited an EMT-like phenotype, compared with control and empty-vector cells, with decreased expression of
E-cadherin accompanied by increased expression of
N-cadherin,
vimentin and α-SMA. Overexpression of CXCL8 activated the PI3K/Akt/NF-κB pathway by promoting the phosphorylation of PI3K, Akt and NF-κB. Subcutaneous
tumors were generated by
subcutaneous injection of LoVo parental cells or CXCL8-transfected LoVo cells in BALB/c nude mice. The
tumor growth was more rapid in the CXCL8-transfected group than that noted in the parental cell group. In conclusion, overexpression of CXCL8 induced cell proliferation, migration and invasion of
colon cancer LoVo cells. CXCL8 may act through induction of EMT via the PI3K/AKT/NF-κB signaling axis.