Chemokines and cytokines: Axis and allies in prostate cancer pathogenesis

Semin Cancer Biol. 2022 Nov;86(Pt 3):497-512. doi: 10.1016/j.semcancer.2022.02.017. Epub 2022 Feb 16.

Abstract

Chemokines are recognized as the major contributor to various tumorigenesis, tumor heterogeneity, and failures of current cancer therapies. The tumor microenvironment (TME) is enriched with chemokines and cytokines and plays a pivotal role in cancer progression. Chronic inflammation is also considered an instructive process of cancer progression, where chemokines are spatiotemporally secreted by malignant cells and leukocyte subtypes that initiate cell trafficking into the TME. In various cancers, prostate cancer (PCa) is reported as one of the leading cancers in the worldwide male population. The chemokines-mediated signaling pathways are intensively involved in PCa progression and metastasis. Emerging evidence suggests that chemokines and cytokines are responsible for the pleiotropic actions in cancer, including the growth, angiogenesis, endothelial mesenchymal transition, leukocyte infiltration, and hormone escape for advanced PCa and therapy resistance. Chemokine's system and immune cells represent a promising target to suppress tumorigenic environments and serve as potential therapy/immunotherapy for the PCa. In this review, an attempt has been made to shed light on the alteration of chemokine and cytokine profiles during PCa progression and metastasis. We also discussed the recent findings of the diverse molecular signaling of these circulating chemokines and their corresponding receptors that could become future targets for therapeutic management of PCa.

Keywords: Chemokines; Cytokines; Prostate cancer; Tumor microenvironment.

Publication types

  • Review
  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Carcinogenesis
  • Chemokines / metabolism
  • Cytokines*
  • Humans
  • Immunotherapy
  • Male
  • Prostatic Neoplasms* / genetics
  • Prostatic Neoplasms* / metabolism
  • Tumor Microenvironment

Substances

  • Cytokines
  • Chemokines