[IL-6 promotes gastric cancer cell proliferation and EMT through regulating miR-152/PIK3R3 pathway]

To explore the role of interleukin (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, Snail1 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, Snail1, 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.