Inflammatory and microenvironmental factors involved in breast cancer progression

摘要

The primary reason for the high mortality rate of breast cancer is metastasis, which can result in a poor survival rate. The tumor environment is important for promotion and invasion of cancer cells. Recent studies have shown that inflammation is associated with breast cancer. Therefore, it is important to investigate the role of the inflammatory and microenvironment in breast cancer progression and metastasis. The present review summarizes some of the markers for inflammation and breast cancer invasion, which may aid in the design of an appropriate therapy for metastatic breast cancer. The following four inflammatory markers are discussed in this review: (1) Tumor associated macrophages (TAMs); (2) Matrix metalloproteinases (MMPs); (3) Sphingosine 1-phosphate (S1P); (4) C-reactive protein (CRP). TAMs are commonly found in breast cancer patients, and high infiltration is positively correlated with poor prognosis and low survival rate. MMPs are well-known for their roles in the degradation of ECM components when cancer cells invade and migrate. MMPs are also associated with inflammation through recruitment of a variety of stromal cells such as fibroblasts and leukocytes. S1P is an inflammatory lipid and is involved in various cellular processes such as proliferation, survival, and migration. Recent studies indicate that S1P participates in breast cancer invasion in various ways. CRP is used clinically to indicate the outcome of cancer patients as well as acute inflammatory status. This review summarizes the current understanding on the role of S1P in CRP expression which promotes the breast epithelial cell invasion, suggesting a specific mechanism linking inflammation and breast cancer. The present review might be useful for understanding the relationship between inflammation and breast cancer for the development of pharmacological interventions that may control the primary molecules involved in the breast cancer microenvironment.