CCL5 promotes the proliferation and metastasis of bladder cancer via the JAK2/STAT3 signaling pathway

CCL5通过JAK2/STAT3信号通路促进膀胱癌增殖和转移

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作者:Jie Shen, Cheng Chen, Zhen Chen, Pengfeng Gong, Lui Shiong Lee, Benjamin N Schmeusser, Qianfeng Zhuang, Yangyang Sun, Dong Xue, Xiaozhou He

Background

Non-muscle invasive bladder cancer (NMIBC) is one of the most common malignant tumors of the urinary system. There is an urgent need for further studies to elucidate the underlying mechanisms of bladder cancer (BC) progression. It has been observed that C-C chemokine ligand 5 (CCL5) and its receptor C-C chemokine receptor type 5 (CCR5) are expressed abnormally and activated in solid tumors and hematological malignancies, which is gaining increasing attention. However, the underlying mechanism of CCL5 in BC remains unclear.

Conclusions

CCL5 may play an oncogenic role in BC and may also serve as a potential diagnostic and prognostic biomarker.

Methods

The expression levels of CCL5 were analyzed by real-time polymerase chain reaction (RT-PCR) and western blot. Proliferation analysis of cells was carried out using Cell Counting Kit-8 (CCK-8). The assessment of the migration was conducted using a wound-healing assay. A Matrigel-coated transwell chamber was used to test cell invasiveness. A subcutaneous transplantation tumor model and tail vein injection pulmonary metastasis tumor model were used to evaluate the proliferation and metastasis of BC cell in vivo.

Results

This study showed that CCL5 promotes proliferative, migratory, and tumor-growing BC cells in vitro and tumor metastasizing BC cells in vivo. Moreover, we found that the tumor-promotive role of CCL5 is dependent on activation of the JAK2/STAT3 signaling pathway. Conclusions: CCL5 may play an oncogenic role in BC and may also serve as a potential diagnostic and prognostic biomarker.

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