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Serum level of SALL4 in gastric cancer patients and its effect on migration of gastric cancer cells |
LIU Lei1 LI Yan2 GUO Yuanbiao1 |
1.Department of Research Center of Experimental Medicine, the Third People′s Hospital of Chengdu (Second Affiliated Hospital, Chongqing Medical University), Sichuan Province, Chengdu 610031, China;
2.Department of Infectious Diseases, the 42 Hospital of People′s Liberation Army, Sichuan Province, Leshan 614000, China |
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Abstract Objective To investigate the difference of serum SALL4 levels between gastric cancer patients and healthy people, and to explore the role of SALL4 in the progression of gastric cancer. Methods A total of 47 patients with gastric cancer who were treated in the Third People′s Hospital of Chengdu from March 2016 to April 2018 and 29 healthy volunteers who participated in the physical examination were selected. The serum levels of SALL4 were detected by ELISA. The expression of SALL4 in mRNA level and protein level in various gastric cancer cell lines and gastric mucosa cells were analyzed by Real-time PCR and Western blot respectively. The effects of SALL4 on the cell migration and invasion ability were analyzed by siRNA interference. The expression levels of related molecules of epithelial-mesenchymal transition (EMT) were detected by Western blot. Results The serum SALL4 levels in patients with gastric cancer were significantly higher than those in healthy volunteers, and the difference was highly statistically significant (P < 0.0001). The expression of SALL4 mRNA and protein in various gastric cancer cell lines was higher than that in gastric mucosal cell lines. The migration and invasion ability of gastric cancer cells were significantly decreased after interfering SALL4 expression, and the differences were statistically significant (P < 0.05). Decreased expression of SALL4 leaded to the up-regulation of E-cadherin expression and the down-regulation of snail, β-catenin and Wnt3a. Conclusion SALL4 is related to the progression of gastric cancer. It may promote cell migration and invasion by inducing the EMT process in gastric cancer cells.
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