| 项目编号 |
PRJCA033119 |
| 项目标题 |
Residual tumor cells promote metastasis after insufficient radiofrequency ablation by educating CD177hiPAD4hi neutrophils |
| 涉及领域 |
Medical |
| 数据类型 |
Transcriptome or Gene expression
|
| 物种名称 |
Mus musculus
Homo sapiens
|
| 描述信息 |
Radiofrequency ablation (RFA) has been the most promising local treatment for colorectal liver metastases, based on its advantage in obtaining complete tumor destruction. However, tumor progression after RFA still severely restricts patient prognosis, and its molecular mechanism remains to be further explored. Here, we demonstrated that heat-stressed residual tumor cells after insufficient RFA (iRFA) led to lung metastases. Specific Cd177hiPad4hi neutrophils are firstly found as the mainly pro-tumor phenotype in iRFA condition, and neutrophil extracellular traps are produced to accelerate lung metastasis by MEK/ERK signaling pathway. Mechanistically, PPARγ-TG synthesis in residual tumor cells activates P38 signaling pathway and CXCL5 secretion, contributing to Cd177hiPad4hi neutrophil infiltration after iRFA. Furthermore, the specific CD36hi-EM-CTCs with activated lipid metabolism characteristics are found assisting in early identification of residual tumor cells. The study not only provide new targets for improving the efficacy of iRFA but realize its early identification and intervention. |
| 样品范围 |
Monoisolate |
| 发布日期 |
2025-03-05 |
| 出版信息 |
| PubMed ID |
文章标题 |
杂志名称 |
Doi |
发表年份 |
| 41330923
|
Residual tumor cells after insufficient radiofrequency ablation promote lung metastasis by educating CD177 hi PAD4 hi neutrophils
|
Nature Communications
|
10.1038/s41467-025-66897-0
|
2025
|
|
|
| 项目资金来源 |
| 机构 |
项目类型 |
授权项目ID |
授权项目名称 |
| National Natural Science Foundation of China (NSFC)
|
|
82173187
|
|
| National Natural Science Foundation of China (NSFC)
|
|
82002555
|
|
| National Natural Science Foundation of China (NSFC)
|
|
82272635
|
|
|
|
| 提交者 |
Wangjun
Liao (liaowj@smu.edu.cn)
|
| 提交单位 |
Nanfang Hospital, Southern Medical University |
| 提交日期 |
2024-12-03 |
