2. Academic Validation
  3. Tumor-associated macrophage-derived CCL5 promotes chemotherapy resistance and metastasis in prostatic cancer

Tumor-associated macrophage-derived CCL5 promotes chemotherapy resistance and metastasis in prostatic cancer

  • Cell Biol Int. 2021 Oct;45(10):2054-2062. doi: 10.1002/cbin.11630.
Jian Ma 1,  Fuerhaiti Shayiti 1,  Jing Ma 2,  Meng Wei 3,  Tingting Hua 4,  Rong Zhang 1,  Junyan Su 5,  Peng Chen 1
Affiliations

Affiliations

  • 1 Urology Department, Xinjiang Medical University Affiliated Tumor Hospital, Ürümqi, Xinjiang, China.
  • 2 Comprehensive Internal Medicine Department, First Affiliated Hospital of Xinjiang Medical University, Ürümqi, Xinjiang, China.
  • 3 Department of Medical Analysis, Xinjiang Zhizhen Medical Laboratory Science Co., Ltd., Xinjiang, China.
  • 4 Department of Ultrasound, Xinjiang Medical University Affiliated Tumor Hospital, Ürümqi, Xinjiang, China.
  • 5 Department of Medical, Lifehealthcare Clinical Laboratories, Beijing, China.
PMID: 34003531 DOI: 10.1002/cbin.11630
Abstract

The crosstalk between tumor microenvironment and Cancer cells is emerging as a critical determinant in tumor progression. However, the underlying mechanism of tumor microenvironment-induced Cancer development remains controversial. Here, our study provides evidence to suggest that tumor-associated macrophage (TAM) enrichment is found in chemoresistant prostatic tumor tissues. Those TAMs are demonstrated to promote chemoresistance and distant metastasis in prostatic Cancer through secretion of CCL5. Mechanistically, TAM coculture or additional CCL5 can mediate the STAT3-dependent epithelial-mesenchymal transition process, resulting in distant metastasis in prostatic Cancer. Meanwhile, activation of STAT3 induced by CCL5 can mediate upregulation of the transcription factor Nanog, leading to drug resistance. In vivo study further demonstrated that blockade of STAT3 signals significantly reverses chemoresistance and suppresses lung metastasis in colorectal tumor-bearing mice, suggesting a novel strategy for clinical prostatic Cancer treatment.

Keywords

CCL5; STAT3; prostatic cancer; tumor-associated macrophages.

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