Targeting the CCL5/CCR5 axis in tumor-stromal crosstalk to overcome cisplatin resistance in neuroendocrine prostate cancer

Our findings identify the CCL5/CCR5 axis as a key mediator of tumor-stromal crosstalk driving cisplatin resistance in NEPC. Mechanistically, CAF-derived CCL5 activates AKT signaling in tumor cells by promoting the formation of the CCR5/β-arrestin1/p85 complex. Targeting this pathway with maraviroc in combination with cisplatin offers a promising therapeutic strategy for overcoming drug resistance in NEPC.

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Publication Details

Journal
Journal of Experimental & Clinical Cancer Research
Published
2025-10-28
DOI
https://doi.org/10.1186/s13046-025-03552-y
Citations
3
Primary Topic
Chemokine receptors and signaling
Type
article
Field-Weighted Citation Impact
3.14
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article

Targeting the CCL5/CCR5 axis in tumor-stromal crosstalk to overcome cisplatin resistance in neuroendocrine prostate cancer

Jiahua Pan, Yiyi Ji, Jiajin Wu, Zehua Ma et al.
3 citations
Journal of Experimental & Clinical Cancer Research
Chemokine receptors and signaling
3.14
article

Targeting the CCL5/CCR5 axis in tumor-stromal crosstalk to overcome cisplatin resistance in neuroendocrine prostate cancer

Jiahua Pan, Yiyi Ji, Jiajin Wu, Zehua Ma, Xinyu Chai, Kai Shen, Xinyu Liu, Weiwei Zhang, Bo Liu, Liang Dong, Cong Hu, Wei Xue, Baijun Dong, Haotian Wu, Zhou Jiang, Yinjie Zhu, Ang Li, Ruopeng Su, Qi Wang
article en
3 citations

Abstract

Our findings identify the CCL5/CCR5 axis as a key mediator of tumor-stromal crosstalk driving cisplatin resistance in NEPC. Mechanistically, CAF-derived CCL5 activates AKT signaling in tumor cells by promoting the formation of the CCR5/β-arrestin1/p85 complex. Targeting this pathway with maraviroc in combination with cisplatin offers a promising therapeutic strategy for overcoming drug resistance in NEPC.

Journal of Experimental & Clinical Cancer ResearchVol. 44(1)
Shanghai Jiao Tong University (CN), Renji Hospital (CN)
Openalex Percentile: Top 7%
Chemokine receptors and signaling
3.14
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