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Background <p>Endosome-associated trafficking regulator 1 (ENTR1), also known as Serologically Defined Colon Cancer Antigen 3 (SDCCAG3), was initially identified in colon cancer and plays a crucial role in protein transport. Preliminary studies indicate that ENTR1 is involved in the growth of certain tumor types.</p> Methods <p>In this study, we analyzed ENTR1 expression levels in normal and tumor tissues using clinical sample data from multiple databases. We also employed Mendelian randomization (MR) analysis of ENTR1. Finally, we conducted in vitro experiments to validate the effects of ENTR1 on colon cancer proliferation and glycolysis.</p> Results <p>Our findings reveal that ENTR1 is upregulated in most tumors. Summary-data-based Mendelian Randomization (SMR) analysis indicates a causal relationship between ENTR1 and colon cancer. Further machine learning and metabolite-based Mendelian randomization suggest that ENTR1 may influence tumor growth by regulating glycolysis. Further cellular experiments confirm that knocking out ENTR1 reduces the proliferation of HCT-116 cells and downregulates the expression levels of key glycolytic enzymes.</p> Conclusions <p>This study uncovers the role of ENTR1 in various cancers and demonstrates that ENTR1 may promote colon cancer growth by regulating glycolysis, providing a new target for cancer therapy.</p> Graphical Abstract <p></p>

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ENTR1 affects the progression of colon cancer by regulating energy metabolism under the influence of glycolysis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月3日

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  • Anquan Ma,
  • Chuanyao Zhai,
  • Qixuan He,
  • Wenhao Wang,
  • Huiping Ren,
  • Kai Mao,
  • Weipeng Lan,
  • Jing Lan

摘要

Background

Endosome-associated trafficking regulator 1 (ENTR1), also known as Serologically Defined Colon Cancer Antigen 3 (SDCCAG3), was initially identified in colon cancer and plays a crucial role in protein transport. Preliminary studies indicate that ENTR1 is involved in the growth of certain tumor types.

Methods

In this study, we analyzed ENTR1 expression levels in normal and tumor tissues using clinical sample data from multiple databases. We also employed Mendelian randomization (MR) analysis of ENTR1. Finally, we conducted in vitro experiments to validate the effects of ENTR1 on colon cancer proliferation and glycolysis.

Results

Our findings reveal that ENTR1 is upregulated in most tumors. Summary-data-based Mendelian Randomization (SMR) analysis indicates a causal relationship between ENTR1 and colon cancer. Further machine learning and metabolite-based Mendelian randomization suggest that ENTR1 may influence tumor growth by regulating glycolysis. Further cellular experiments confirm that knocking out ENTR1 reduces the proliferation of HCT-116 cells and downregulates the expression levels of key glycolytic enzymes.

Conclusions

This study uncovers the role of ENTR1 in various cancers and demonstrates that ENTR1 may promote colon cancer growth by regulating glycolysis, providing a new target for cancer therapy.

Graphical Abstract