[Inhibitory effect of overexpressed kisspeptin on proliferation and migration of MKN-45 gastric cancer cells].

Objective To investigate the expression of kisspeptin in gastric adenocarcinoma and its effect on the proliferation and migration of gastric cancer cells. Methods The level of kisspeptin in 50 gastric cancer tissues and their paracancerous tissues were detected by quantitative real-time PCR and Western blotting. Kisspeptin-siRNA, control-siRNA, pEGFP-N1-kisspeptin, pEGFP-N1 were separately transfected into MKN-45 gastric cancer cells. After 48-hour culture, the levels of matrix metalloproteinase-2 (MMP-2), β-catenin, C-myc, MMP-9, kisspeptin were detected by Western blotting; MTT assay was used to detect the proliferation of MKN-45 cells; wound healing assay was performed to assess the migration ability of MKN-45 cells. After MKN-45 cells were treated with Wnt/β-catenin signal pathway inhibitor FH535, MTT assay and flow cytometry were used to evaluate cell proliferation ability and cell apoptosis, respectively. Results Kisspeptin expression in gastric adenocarcinoma tissues was significantly lower than that of the adjacent normal tissues. The cell survival rate and migration rate of pEGFP-N1-kisspeptin group were significantly lower than those of pEGFP-N1 group. Cell survival rate and migration rate of kisspeptin-siRNA group were significantly higher than those of control siRNA group. The levels of MMP-9, MMP-2, β-catenin and C-myc in pEGFP-N1-kisspeptin group were significantly lower than those in pEGFP-N1 group. The levels of MMP-9, MMP-2, β-catenin and C-myc in kisspeptin-siRNA group were significantly higher than those in control-siRNA group. The proliferation and migration trend of gastric cancer cells treated with FH535 was similar to that of the pEGFP-N1-kisspeptin group. Conclusion The expression of kisspeptin decreases in gastric cancer tissues, and kisspeptin can interact with Wnt/β-catenin signaling pathway to inhibit the proliferation and migration of gastric cancer cells.