ETV7 promotes 5-FU resistance and malignant progression through CXCL1-induced NETs formation in colorectal cancer

Resistance to 5-fluorouracil (5-FU) remains a major challenge in the treatment of colorectal cancer (CRC). Here, we identify ETS variant transcription factor 7 (ETV7) as significantly upregulated in CRC tissues and cell lines, with elevated expression associated with poor clinical prognosis. Functional assays demonstrate that ETV7 enhances CRC cell proliferation, invasion, and resistance to 5-FU. Mechanistically, ETV7 transcriptionally upregulates CXCL1, leading to increased neutrophil recruitment and enhanced formation of neutrophil extracellular traps (NETs). The resulting NETs-enriched tumor microenvironment promotes tumor aggressiveness and chemoresistance. Pharmacological inhibition of CXCL1 or degradation of NETs effectively attenuates ETV7-driven malignant phenotypes in vitro and in vivo. Collectively, these findings establish an ETV7-CXCL1-NETs axis that contributes to 5-FU resistance in CRC and suggest that targeting this pathway may improve chemotherapy response.

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Publication Details

Journal
Communications Biology
Published
2026-03-31
DOI
https://doi.org/10.1038/s42003-026-09976-2
Primary Topic
Chemokine receptors and signaling
Type
article
Field-Weighted Citation Impact
0.00

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article

ETV7 promotes 5-FU resistance and malignant progression through CXCL1-induced NETs formation in colorectal cancer

Huabin Gao, Shuang Mo, Jianqiang Wu, Yongrui Lv et al.
Communications Biology
Chemokine receptors and signaling
article

ETV7 promotes 5-FU resistance and malignant progression through CXCL1-induced NETs formation in colorectal cancer

Huabin Gao, Shuang Mo, Jianqiang Wu, Yongrui Lv, LEI LIU, Lixia Chen, Pei Xia, Shujin He, Lin Chen
article en

Abstract

Resistance to 5-fluorouracil (5-FU) remains a major challenge in the treatment of colorectal cancer (CRC). Here, we identify ETS variant transcription factor 7 (ETV7) as significantly upregulated in CRC tissues and cell lines, with elevated expression associated with poor clinical prognosis. Functional assays demonstrate that ETV7 enhances CRC cell proliferation, invasion, and resistance to 5-FU. Mechanistically, ETV7 transcriptionally upregulates CXCL1, leading to increased neutrophil recruitment and enhanced formation of neutrophil extracellular traps (NETs). The resulting NETs-enriched tumor microenvironment promotes tumor aggressiveness and chemoresistance. Pharmacological inhibition of CXCL1 or degradation of NETs effectively attenuates ETV7-driven malignant phenotypes in vitro and in vivo. Collectively, these findings establish an ETV7-CXCL1-NETs axis that contributes to 5-FU resistance in CRC and suggest that targeting this pathway may improve chemotherapy response.

Communications BiologyVol. 9(1)
Sun Yat-sen University (CN), Panyu District Central Hospital (CN), The First Affiliated Hospital, Sun Yat-sen University (CN), Southern Medical University (CN), Guangzhou Medical University (CN)
National Natural Science Foundation of China, China Postdoctoral Science Foundation, Postdoctoral Research Foundation of China
Good health and well-being
Openalex Percentile: Top 43%
Chemokine receptors and signaling
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ETV7 promotes 5-FU resistance and malignant progression through CXCL1-induced NETs formation in colorectal cancer — Huabin Gao, Shuang Mo, et al. · Communications Biology (2026) | TGRS Research Map | TGRS