CER1 as a manganese ion metabolism gene drives gastric cancer progression and therapeutic potential via oxidative stress and tumor microenvironment regulation.

Abstract

Background: Metal ions are vital for biological regulation and contribute to gastric cancer (GC) development, but the mechanisms are unclear. This study investigates the role of the manganese ion metabolism (MIM)-related gene CER1 in GC, focusing on how CER1 induces oxidative stress, contributes to tumor microenvironment heterogeneity, and its potential for targeted personalized therapy.

Methods: Using single-cell RNA sequencing and multi-omics technologies, we characterized molecular subtypes of gastric cancer (GC) and explored the biological roles of the MIM family, elucidating genetic mechanisms of GC initiation and immune dysregulation.

Results: Our analysis systematically clarified the pivotal role of the MIM gene family in GC, and revealed that CER1 promoted T cell exhaustion and facilitated immune evasion. The bioinformatics analysis indicated that CER1 may regulate tumor cell biological behavior through the NRF2/KEAP1-mediated oxidative stress signaling pathway. In summary, CER1, as a member of the MIM family, serves as a central hub in the oxidative stress and immune regulation.

Conclusion: The in-depth investigation of CER1 within the MIM family has markedly deepened our understanding of the complex molecular mechanisms underlying GC. Through targeted manipulation of the NRF2/KEAP1 oxidative stress pathway and T cell function, CER1 emerges as a strategic pathway for potentially inhibiting tumor growth. This investigation outlines a strategic framework to facilitate the advancement of innovative treatment modalities.