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Background <p>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.</p> Methods <p>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.</p> Results <p>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.</p> Conclusion <p>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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月22日

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  • Juan Hu,
  • Ruian Zhu,
  • Qiushi Huang,
  • Xiaosong Li

摘要

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.