Skip to main content
Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Helicobacter pylori CagA promotes epithelial mesenchymal transition in gastric carcinogenesis via triggering oncogenic YAP pathway

Fig. 2

Increase of YAP in concert with a decrease of E-cadherin was positively correlated with progression of the histopathological cascade of human gastric cancer and H. pylori infection was associated with higher levels of YAP and lower levels of E-cadherin in the chronic non-atrophic gastritis (CNAG) tissues compared with those in H. pylori CNAG subjects. a, b Representative images of Immunohistochemical staining for YAP and E-cadherin in human gastric tissues (Magnification 200×, bars =50 μm). Serial tissues were harvested from human gastric mucosa with CNAG, intestinal metaplasia (IM), dysplasia (Dys), gastric carcinoma (GC). Scores were evaluated and statistically compared for expression of YAP (c) and E-cadherin (d). e Pearson correlation indicated that there was a negative correlation between the expression scores of YAP and E-cadherin score (r2 = 0.464, p < 0.01). Expression levels of YAP (f) and E-cadherin (g) was compared between H. pylori+ and H. pylori gastric tissues with different stages (CNAG, IM, Dys, GC) of the Correa histopathological cascade

Back to article page