Key Factor Regulating Inflammatory Microenvironment, Metastasis, and Resistance in Breast Cancer: Interleukin-1 Signaling

Author:

Liu Fengjie1ORCID,Li Lihong1,Lan Meng1,Zou Tengteng1,Kong Zhaodi1,Cai Tiange2ORCID,Wu Xiao Yu3ORCID,Cai Yu14ORCID

Affiliation:

1. College of Pharmacy, Jinan University, Guangzhou 510632, China

2. College of Life Sciences, Liaoning University, Shenyang 110036, China

3. Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, M5S 3M2, Canada

4. Guangdong Key Lab of Traditional Chinese Medicine Information Technology, Guangzhou 510632, China

Abstract

Breast cancer is one of the top-ranked cancers for incidence and mortality worldwide. The biggest challenges in breast cancer treatment are metastasis and drug resistance, for which work on molecular evaluation, mechanism studies, and screening of therapeutic targets is ongoing. Factors that lead to inflammatory infiltration and immune system suppression in the tumor microenvironment are potential therapeutic targets. Interleukin-1 is known as a proinflammatory and immunostimulatory cytokine, which plays important roles in inflammatory diseases. Recent studies have shown that interleukin-1 cytokines drive the formation and maintenance of an inflammatory/immunosuppressive microenvironment through complex intercellular signal crosstalk and tight intracellular signal transduction, which were found to be potentially involved in the mechanism of metastasis and drug resistance of breast cancer. Some preclinical and clinical treatments or interventions to block the interleukin-1/interleukin-1 receptor system and its up- and downstream signaling cascades have also been proven effective. This study provides an overview of IL-1-mediated signal communication in breast cancer and discusses the potential of IL-1 as a therapeutic target especially for metastatic breast cancer and combination therapy and current problems, aiming at enlightening new ideas in the study of inflammatory cytokines and immune networks in the tumor microenvironment.

Funder

Natural Science Foundation of Guangdong Province

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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