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Regulation of epithelial-mesenchymal transition by MACC1 via the HGF/c-Met signaling pathway and its effects on ability of migration and invasion of gastric carcinoma cells

ZHU Qian-qian1, SHAN Hai-xia2, ZHU Zheng-qiu2   

  1. 1.School of Postgraduate, Xuzhou Medical College, Xuzhou 221002， China； 2.Department of Oncology, the Affiliated Hospital of Xuzhou Medical College, Xuzhou 221002, China
  • Online:2014-09-28 Published:2014-09-26
  • Supported by:

    Jiangsu Province Department of Health Project, H201323

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Abstract:

Objective To investigate the regulatory effect of metastasis-associated gene in colon cancer-1 (MACC1) on the epithelial-mesenchymal transition (EMT) by regulating the HGF/c-Met signaling pathway and the effects of MACC1 on the migration and invasion of gastric carcinoma cells. Methods Short hairpin RNA (shRNA) plasmid vector that targeted MACC1 and c-Met (MACC1-shRNA and c-Met-shRNA) and negative control plasmid (shNC) were constructed and transfected into the human gastric carcinoma MKN28 cell line by the lipofectamine technique. The variations of expressions of proteins and mRNA of markers (E-cadherin and N-cadherin) related to MACC1, c-Met, and EMT before and after the transfection were detected by the Western blotting and Real-Time PCR. The variations of the ability of migration and invasion of MKN28 cells were detected by the wound-healing and Transwell invasion tests. Results Compared to the blank control group, the expressions of proteins and mRNA of MACC1 and c-Met of the MACC1-shRNA group were significantly down-regulated (P<0.01); the expressions of protein and mRNA of E-cadherin were significantly up-regulated (P<0.01); and the expressions of protein and mRNA of N-cadherin were significantly down-regulated (P<0.01). The expressions of protein and mRNA of MACC1 of the c-Met-shRNA group did not change significantly (P>0.05) and the variations of expressions of EMT related markers were consistent with those of the MACC1-shRNA group. The results of wound-healing and Transwell invasion tests showed that compared to the blank control group, the ability of migration and invasion of MKN28 cells of the MACC1-shRNA group and c-Met-shRNA group was significantly inhibited (P<0.01). Conclusion MACC1 may regulate the EMT process by regulating the HGF/c-Met signaling pathway and enhance the ability of migration and invasion of gastric carcinoma cells.

Key words: gastric carcinoma, metastasis-associated in colon cancer-1, HGF/c-Met signaling pathway, epithelial-mesenchymal transition, migration, invasion