SALL4 may promote gastric cancer invasiveness in presence of Helicobacter pylori infection

Gastric cancer (GC) is the third cause of cancer-related death worldwide. One of the most important environmental factors of GC is Helicobacter pylori infection. H. pylori affects the gene expression level in multiple cellular pathways. The main objective of this work was to explore the correlation between SALL4 gene expression and H. pylori infection in the GC patients.Method and MaterialThe mRNA level of SALL4 was studied in 74 fresh-frozen tumoral and margin-normal tissues of GC patients using real-time PCR. All the samples were also checked for H. Pylori infection. Data were analyzed using the SPSS22 statistical package.Results The overexpression of SALL4 was observed in 43.2% (32 of 74) of GCs while its underexpression was observed in 18.9 % (14 of 74) of samples. 40 out of 74 patients were H. pylori positive while other were H. pylori-negative. A significant correlation was observed between SALL4 expression and lymph node metastasis (P value= 0.041). However, there was no significant correlation between H. pylori infection and SALL4 expression. The overexpression of SALL4 was inversely correlated to depth of tumor invasion (P =0.022), tumor size (P = 0.041), and stage of tumor progression (P = 0.05) in patients without H. pylori infection.Conclusion SALL4 overexpression may play role in lymph node metastasis of GC. It also may be extrapolated that SALL4 overexpression may cause tumor progression in the presence of the H. pylori infection, suggesting an important role for H. pylori in inducing SALL4 and therefore stemness state of GC.

کلیدواژه ها:

Gastric cancer ، SALL4 ، H.Pylori ، CSC ، Stemness