Expression and clinical significance of autophagic protein LC3B and EMT markers in gastric cancer

Abstract

Background and aim

Gastric cancer (GC) is a fatal malignancy with high rate of recurrence and metastasis. Here, we investigated the correlations between the expression of autophagic protein LC3B and 2 epithelial–mesenchymal transition-related proteins (E-cadherin and Vimentin) and the clinicopathological factors and prognosis of patients with GC.

Materials and methods

The expression of LC3B, E-cadherin, and Vimentin in GC samples (110 cases) and paracarcinoma tissues (40 cases) was analyzed using the Oncomine databases and further detected by immunohistochemistry. The correlations among these markers expression and clinicopathological features in GC were analyzed. The patients were followed for survival analysis.

Results

Compared to the nontumor tissues, the expression of LC3B and Vimentin proteins were significantly elevated in GC tissues, but the E-cadherin expression was decreased (all p<0.05). Interestingly, LCB expression was positively correlated with Vimentin ( r=0.320, p=0.001) and negatively associated with E-cadherin expression ( r= −0.484, p<0.001) in GC. The expression of these markers was closely related to tumor differentiation, T classification, TNM stage, and lymph node metastasis (all p<0.05). Furthermore, survival analyses and screening Kaplan–Meier plotter database revealed that GC patients with high LC3B and Vimentin expression levels had a poorer clinical outcome than those with low expression. Conversely, high E-cadherin expression was linked with favorable overall survival (all p<0.05, log-rank test). Multivariate survival analysis demonstrated that LC3B, E-cadherin, and Vimentin expression were independent prognostic factors of GC patients.

Conclusion

LC3B, E-cadherin, and Vimentin may play an important role in the tumorigenesis of GC, and these marker expressions may serve as additional prognostic indicators for overall survival of patients. The interactions of autophagy and epithelial–mesenchymal transition in GC merits further investigation.