生物
技术
宫颈癌
串扰
放射治疗
癌症研究
肿瘤科
癌症
内科学
医学
遗传学
天文
电离层
光学
物理
作者
Qingyu Huang,Wenhui Yang,Fuhao Wang,Rui Huang,Qian Wang,Xiaohui Li,Tianyu Lei,Shengqin Yue,Wenxue Zou,Qi An,Jinbo Yue,Qinyong Hu,Chao Liu
标识
DOI:10.1186/s12943-025-02244-7
摘要
P-selectin (SELP) expression in tumor cells has been implicated in promoting tumor progression and treatment resistance across various cancers. However, our prior study identified SELP expression in a specific subpopulation of endothelial cells within cervical cancer (CC) and potentially linked to anti-cancer immune response. The precise mechanisms by which SELP influences anti-cancer immunity and its involvement in radiotherapy response in CC, however, remain elusive. To address these gaps, this study analyzed tumor tissue samples from 205 CC patients undergoing radiotherapy, scRNA-seq data from 42,159 cells of eight patients, and bulk RNA-sequencing data from 187 radiotherapy-treated patients. The results revealed that elevated SELP expression in tumor endothelial cells (TECs) was significantly correlated with improved survival outcomes in patients treated with radiotherapy. The SELPhigh group exhibited a prominent enrichment of immune-related pathways, coupled with a diminished enrichment in epithelial cell proliferation and angiogenesis pathways. Notably, this group demonstrated increased infiltration of CD8+ T cells and enhanced expression of chemokine receptors, including ACKR1. Furthermore, our data suggest that SELP+ TECs engage in crosstalk with CD8+ T cells via the ACKR1-CCL5 axis, which is associated with improved radiotherapy efficacy. In conclusion, these findings underscore the pivotal role of SELP+ TEC:CD8+ T cell interactions through the ACKR1-CCL5 pathway in enhancing radiotherapy response in CC. Targeting this crosstalk may offer novel therapeutic strategies to mitigate treatment resistance and improve patient survival.
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