CXCR4/CXCL12 blockade therapy; a new horizon in TNBC therapy

Abdulrahman Qais Khaleel1, Farag M A Altalbawy2, Majid S Jabir3

  • 1Department of Medical Instruments Engineering, Al-Maarif University College, Al Anbar, 31001, Iraq. abdulrahman.qais@uoa.edu.iq.

Insights

Triple-negative breast cancer (TNBC) lacks targeted therapies. The CXCR4/CXCL12 axis plays a key role in TNBC progression and therapy resistance, offering potential new treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapies, accounting for 15-20% of breast cancer cases.
  • The tumor microenvironment (TME), comprising nonmalignant cells, extracellular matrix, and soluble factors like cytokines, significantly influences TNBC development and therapy resistance.
  • Chemokines, such as the CXCL12/CXCR4 axis, are increasingly recognized for their critical roles in TNBC pathophysiology.

Purpose of the Study:

  • To review the multifaceted role of the CXCR4/CXCL12 axis in triple-negative breast cancer.
  • To elucidate the involvement of this axis in TNBC development, metastasis, angiogenesis, and acquired treatment resistance.
  • To summarize current literature on targeting the CXCR4/CXCL12 axis for potential therapeutic interventions in TNBC.

Main Methods:

  • Literature review synthesizing findings from preclinical and clinical studies.
  • Analysis of the molecular mechanisms underlying CXCR4/CXCL12 signaling in TNBC.
  • Compilation of data on therapeutic strategies targeting the CXCR4/CXCL12 axis.

Main Results:

  • The CXCR4/CXCL12 axis is implicated in promoting TNBC cell proliferation and survival.
  • This axis facilitates tumor angiogenesis and the formation of a pro-metastatic microenvironment.
  • CXCR4/CXCL12 signaling contributes to resistance against various cancer therapies.

Conclusions:

  • The CXCR4/CXCL12 axis is a critical regulator of TNBC progression and therapeutic response.
  • Targeting the CXCR4/CXCL12 axis represents a promising strategy for developing novel treatments for TNBC.
  • Further research into this axis may uncover new therapeutic targets and combination strategies for improved patient outcomes.

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