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CCL5 促进肾癌循环肿瘤细胞的上皮间质转化。

CCL5 promotes the epithelial-mesenchymal transition of circulating tumor cells in renal cancer.

机构信息

Department of Urology, School of Medicine, The Second Affiliated Hospital, Xi'an Jiaotong University, No 157 Xiwu Road, Xi'an, 710004, Shaan Xi, China.

Department of Urology, The First Affiliated Hospital, Zhengzhou University, No 1 Jianshe East Road, Zhengzhou, 450052, He Nan, China.

出版信息

J Transl Med. 2024 Sep 3;22(1):817. doi: 10.1186/s12967-024-05297-2.

DOI:10.1186/s12967-024-05297-2
PMID:39227943
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11370314/
Abstract

BACKGROUND

Circulating tumor cells (CTCs) are pivotal in tumor metastasis across cancers, yet their specific role in renal cancer remains unclear.

METHODS

This study investigated C-C motif chemokine ligand 5 (CCL5)'s tumorigenic impact on renal cancer cells and CTCs using bioinformatics, in vivo, and in vitro experiments. It also assessed renal cancer patients' CTCs prognostic value through Lasso regression and Kaplan-Meier survival curves.

RESULTS

Bioinformatics analysis revealed differential genes focusing on cellular adhesion and migration between CTCs and tumor cells. CCL5 exhibited high expression in various CTCs, correlating with poor prognosis in renal cancer. In 786-O-CTCs, CCL5 enhanced malignancy, while in renal cell carcinoma cell line CAKI-2 and 786-O, it promoted epithelial-mesenchymal transition (EMT) via smad2/3, influencing cellular characteristics. The nude mouse model suggested CCL5 increased CTCs and intensified EMT, enhancing lung metastasis. Clinical results shown varying prognostic values for different EMT-typed CTCs, with mesenchymal CTCs having the highest value.

CONCLUSIONS

In summary, CCL5 promoted EMT in renal cancer cells and CTCs through smad2/3, enhancing the malignant phenotype and facilitating lung metastasis. Mesenchymal-type CTC-related factors can construct a risk model for renal cancer patients, allowing personalized treatment based on metastatic risk prediction.

摘要

背景

循环肿瘤细胞（CTCs）在癌症转移中起着关键作用，但它们在肾癌中的具体作用尚不清楚。

方法

本研究通过生物信息学、体内和体外实验，研究了 C-C 基序趋化因子配体 5（CCL5）对肾癌细胞和 CTCs 的致瘤作用。还通过 Lasso 回归和 Kaplan-Meier 生存曲线评估了肾癌患者 CTCs 的预后价值。

结果

生物信息学分析显示，CTC 与肿瘤细胞之间的差异基因集中在细胞黏附和迁移上。CCL5 在各种 CTCs 中表达较高，与肾癌预后不良相关。在 786-O-CTC 中，CCL5 增强了恶性程度，而在肾癌细胞系 CAKI-2 和 786-O 中，它通过 smad2/3 促进上皮-间充质转化（EMT），影响细胞特征。裸鼠模型表明 CCL5 增加了 CTCs 并加剧了 EMT，增强了肺转移。临床结果表明，不同 EMT 型 CTCs 的预后价值不同，间充质 CTCs 的价值最高。

结论

总之，CCL5 通过 smad2/3 促进了肾癌细胞和 CTCs 的 EMT，增强了恶性表型并促进了肺转移。间充质型 CTC 相关因素可以为肾癌患者构建风险模型，根据转移风险预测进行个体化治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/941a6a5db419/12967_2024_5297_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/2c67bb6d63a0/12967_2024_5297_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/eadab687bdd9/12967_2024_5297_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/ea57157cb2f5/12967_2024_5297_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/0accc0e47bb7/12967_2024_5297_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/0b8608e6d039/12967_2024_5297_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/941a6a5db419/12967_2024_5297_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/2c67bb6d63a0/12967_2024_5297_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/eadab687bdd9/12967_2024_5297_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/ea57157cb2f5/12967_2024_5297_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/0accc0e47bb7/12967_2024_5297_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/0b8608e6d039/12967_2024_5297_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd06/11370314/941a6a5db419/12967_2024_5297_Fig6_HTML.jpg

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