CXCL12-CXCR4/CXCR7 Axis in Cancer: from Mechanisms to Clinical Applications.

Int J Biol Sci

Department of Orthopedics, Shenmu Hospital, Faculty of Life Sciences and Medicine, Northwest University, Shenmu, China.

Published: August 2023

AI Article Synopsis

  • Cancer is caused by a series of genetic mutations and epigenetic changes, posing a major global health challenge.
  • Cytokines and chemokines, particularly the CXCL12-CXCR4/CXCR7 signaling pathway, are crucial in cancer development, affecting processes like tumor growth and spread.
  • This review focuses on the latest findings about the CXCL12-CXCR4/CXCR7 interactions and their potential as biomarkers or targets for new cancer therapies.

Article Abstract

Cancer is a multi-step disease caused by the accumulation of genetic mutations and/or epigenetic changes, and is the biggest challenge around the world. Cytokines, including chemokines, exhibit expression changes and disorders in all human cancers. These cytokine abnormalities can disrupt homeostasis and immune function, and make outstanding contributions to various stages of cancer development such as invasion, metastasis, and angiogenesis. Chemokines are a superfamily of small molecule chemoattractive cytokines that mediate a variety of cellular functions. Importantly, the interactions of chemokine members CXCL12 and its receptors CXCR4 and CXCR7 have a broad impact on tumor cell proliferation, survival, angiogenesis, metastasis, and tumor microenvironment, and thus participate in the onset and development of many cancers including leukemia, breast cancer, lung cancer, prostate cancer and multiple myeloma. Therefore, this review aims to summarize the latest research progress and future challenges regarding the role of CXCL12-CXCR4/CXCR7 signaling axis in cancer, and highlights the potential of CXCL12-CXCR4/CXCR7 as a biomarker or therapeutic target for cancer, providing essential strategies for the development of novel targeted cancer therapies.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10367567PMC
http://dx.doi.org/10.7150/ijbs.82317DOI Listing

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