ALDOC regulated the biological function and immune infiltration of gastric cancer cells

Int J Biochem Cell Biol. 2023 May:158:106407. doi: 10.1016/j.biocel.2023.106407. Epub 2023 Mar 30.

Abstract

Background: The role of ALDOC which is an important regulator involved in tumor metabolic reprogramming and immune microenvironment in GC remains unclear. Therefore, we investigated the feasibility of ALDOC as a prognostic marker and therapeutic target.

Methods: We verified the expression of ALDOC in GC and its effect on the prognosis of GC patients by analyzing clinical data. The regulation of ALDOC on the biological behavior of GC cells was confirmed by experiments. The potential mechanism of miRNA regulating GC immune cell infiltration by inhibiting ALDOC was explored by experiments and bioinformatic analysis. We further analyzed the effect of ALDOC on somatic mutations in gastric cancer, and constructed a prognostic model based on ALDOC and related immune molecules.

Results: ALDOC is overexpressed in GC cells and tissues, which promotes malignant biological behavior of GC cells and is an independent risk factor for poor prognosis of GC patients. MiR-19a-5p promotes the expression of ALDOC by down-regulating ETS1, leading to poor prognosis in GC patients. ALDOC is significantly associated with immune infiltration in GC, regulates macrophage differentiation and promotes the progression of GC. ALDOC is significantly correlated with TMB and MSI of gastric cancer, and affects somatic mutation of gastric cancer. The prognostic model has good predictive efficiency.

Conclusions: ALDOC is a potential prognostic marker and therapeutic target with abnormal immune-mediated effects. The prognostic model based on ALDOC provides a reference for prognosis prediction and individualized treatment of GC patients.

Keywords: ALDOC; Immune infiltration; Neoplasm; Prognosis; Stomach.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Gene Expression Regulation, Neoplastic
  • Humans
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Stomach Neoplasms* / genetics
  • Stomach Neoplasms* / pathology
  • Tumor Microenvironment / genetics

Substances

  • MicroRNAs