Differential expression of COL6 family is a potential tumor marker for predicting gastric cancer

Abstract Background Gastric cancer (GC) is one of the most common cancers in the worldwide and is the leading cause of death in patients. Despite significant advances in treatment, the 5-year survival rate remains low. Therefore, the discovery of tumor markers that can predict gastric cancer and estimate its prognosis will improve this situation. Methods In this study, TIMER2, Kaplan–Meier plotter and GEPIA databases were used to analyze the expression of COL6 family gene in gastric cancer tissues, and analyzed their relationship with different pathological stages and tumor prognosis. Meanwhile, we analyzed the Genetic Alteration, Co-expression, Neighbor Gene Network, Interaction Analyses, enrichment analysis and immune infiltration analysis of COL6 in Patients with GC in cBioPortal, STRING databases and XIANTAO platform. Results We found that the COL6 family (COL6A1, COL1A2, COL6A3, COL6A4P1, COL6A4P2, COL6A5 and COL6A6) genes were significantly up-regulated in gastric adenocarcinoma relative to normal tissue adjacent to the cancer. A significant correlation was found between the expression of COL6A1/2/3 and the pathological stage of GC patients. GC patients with high COL6A1/2/3/5/6 expression were all associated with poor survival, while COL6A4P1/P2/6 were significantly associated with metastasis or recurrence in patients. Subsequently, we performed functional enrichment analysis and found that its cellular function was associated with Focal adhesion, ECM-receptor interaction. Our data also showed that COL6A1/2/3/5/6 were positively with immune infiltration, while a negative correlation was found between COL6A/4P1/4P2 and immune cells infiltration, which may be associated with poorer relapse-free survival (RFS). Conclusion Our findings suggest that the COL6 family (COL6A1/2/3/4P1/4P2/5/6) is a potential biomarker for determining the prognosis of gastric cancer and It also provides theoretical basis for immunotherapy.