Unveiling the role of taurine and SLC6A6 in tumor immune evasion: Implications for gastric cancer therapy microbiology

https://doi.org/10.1016/j.biocel.2024.106661Get rights and content

Abstract

Metabolic changes are key drivers of tumor progression. Understanding how metabolic reprogramming promotes tumor development and identifying key metabolic activities are essential for improving tumor diagnosis and treatment. Among the numerous transporters in the body, solute carriers (SLCs) are particularly significant, often overexpressed in cancer cells to meet the tumor’s demand for nutrients and energy. While the role of SLCs in nutrient absorption within the gastrointestinal tract is well-established, their specific role in gastric cancer (GC) remains unclear. Recently, Xiaodi Zhao’s team investigated the critical role of taurine and its transporter, SLC6A6, in anti-tumor immunity and clinical outcomes. Notably, this research marks the first instance of taurine exhibiting a dual role. It promotes tumor growth in immunodeficient mice while inhibiting it in immunocompetent mice. The study found that taurine exerts its anti-cancer effects by modulating CD8+ T cells rather than directly inhibiting tumor cells, revealing the SP1-SLC6A6 axis as a key mechanism behind chemotherapy-induced immune evasion. Our work further explored the potential, advantages, and challenges of using taurine and SLC6A6 as biomarkers and therapeutic targets in gastric cancer. We aim to underscore their importance in both basic research and clinical applications, providing valuable insights and guidance for future investigations.

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CRediT authorship contribution statement

Jianqiao Shentu: Writing – original draft, Visualization, Conceptualization. Xinming Su: Visualization. Shiwei Duan: Writing – review & editing, Project administration, Funding acquisition, Conceptualization. Yueqi Yu: Visualization.

Author contributions

JS analyzed the literature and wrote the manuscript. JS, XS, and YY drafted the figure. JS and SD conceived the idea. SD reviewed and revised the manuscript. All authors gave the final approval of the submitted version.

Consent for publication

All authors have read and agreed to the published version of the manuscript.

Ethics approval and consent to participate

Not applicable.

Funding source

This study was supported by the Qiantang Scholars Fund in Hangzhou City University (No. 210000-581835).

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Acknowledgments

The authors would like to thank PubMed for the valuable information. Figure was created by BioRender (https://app.biorender.com).

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© 2024 Published by Elsevier Ltd.

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