IL-6 promotes gastric cancer cell proliferation and EMT through regulating miR-152/PIK3R3 pathway / 中南大学学报(医学版)

ABSTRACT

Objective:To explore the role ofinterleukin (IL)-6 in gastric cancer cells and the mechanisms.Methods:Gastric cancer cells MGC-803 were treated with 50 ng/mL of recombinant IL-6 protein,and then cell viability and cell migration were detected by MTT assay and wound-healing assay,respectively.The mRNA and protein expressions of E-cadherin,N-cadherin,vimentin,Snaill and miR-152 were analyzed by RT-qPCR and Western blot,respectively.Moreover,MGC-803 cells were simultaneously or separately treated with IL-6 and transfected with miR-152 mimics,and then the mRNA expression of PIK3R3 and the protein levels of PIK3R3,Akt and p-Akt were determined.Results:IL-6 stimulation significantly promoted cell proliferation and migration,reduced the expression of E-cadherin and miR-152,and increased the expression of N-cadherin,vimentin,Snaill,PIK3R3 and p-Akt (All P＜0.05).The protein levels of PIK3R3 and p-Akt were significantly decreased after transfecting miR-152 mimics into MGC-803 cells (P＜0.01).miR-152 overexpression down-regulated IL-6-induced the protein expression of PIK3R3 and p-Akt (P＜0.01).The levels of Akt in each group were not changed.Conclusion:IL-6 up-regulates PIK3R3 expression and activates PI3K/Akt signaling pathway through down-regulating miR-152 expression,which consequently promotes gastric cancer cell proliferation,migration,and epithelial-mesenchymal transition.