A ferroptosis-related gene in Helicobacter pylori infection, SOCS1, serves as a potential prognostic biomarker and corresponds with tumor immune infiltration in stomach adenocarcinoma: In silico approach.

Abstract

Helicobacter pylori (H. pylori) is a major risk factor for the stomach adenocarcinoma (STAD). This study aimed to investigate the potential role of a H. pylori infection-related gene, SOCS1, in STAD. Online available databases were analyzed to determine the expression, correlations with clinicopathologic parameters, patients' survival, and immunological characteristics of SOCS1 in TCGA-STAD or GEO datasets. Univariate and multivariate Cox regression analyses were used to determine independent risk factors, which were further integrated to establish a nomogram. A comparison of drug sensitivity was conducted for the chemotherapy responses between individuals with low- and high-SOCS1. Prediction of tumor response to checkpoint inhibitors was based on the tumor immunodeficiency and exclusion (TIDE) score. SOCS1 expression was significantly increased in both H. pylori-infected and STAD patients. Higher SOCS1 expression indicated an undesirable prognosis in STAD patients. SOCS1 upregulation was related to enhanced immune cell infiltrations and the upregulation of immune checkpoints in STAD patients. N stage, age and SOCS1 were identified as independent risk factors for higher mortality of STAD patients and confirmed using the nomogram. Drug sensitivity analyses demonstrated that high expression of SOCS1 in STAD patients could improve the sensitivity to chemotherapy. TIDE score showed that STAD patients with high SOCS1 expression would have superior response to immunotherapy. SOCS1 may act as a potential biomarker for uncovering the underlying mechanisms of gastric cancer. Increasing the activity of immunotherapy through ferroptosis-immunomodulation may be a viable strategy in STAD therapy.