Abstract

Background: Breast cancer (BC) is the most diagnosed cancer among women worldwide and the second-most cause of women's deaths. The interleukin-1 (IL-1), interleukin-6 (IL-6), and tumour necrosis factor-α (TNF-α) are critical for BC pathogenesis. They participate in BC development and progression by regulating several pathways. The findings of this review paper can potentially guide the development of targeted therapies that can improve the prognosis and treatment outcomes for BC patients. Objective: To make a comprehensive and up-to-date review of the original papers on the role of IL-1, IL-6, and TNF-α in BC development and progression. Method: This literature review is an iterative and objective analysis of the English original papers published in the last five years, which linked IL-1, IL-6, TNF-α, and BC. Result: IL-1, IL-6, and TNF-α significantly affect angiogenesis, proliferation, apoptosis, survival, and metastatic in BC by regulating the PI3K-PKB/Akt, JNK, IL-6/JAK/STAT3, Ras/Raf, AKT, MAPK, and NF-κB pathways. They also modulate the TME by promoting the production of extracellular matrix components and stimulating the recruitment of immune cells. Conclusion: Inhibiting IL-1, IL-6, and TNF-α and their downstream signalling intermediates could be promising strategies for suppressing BC development and progression. Further in-depth research is necessary to develop novel targeted therapies and improve patient outcomes.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.