A Cell-Based Systematic Review on the Role of Annexin A1 in Triple-Negative Breast Cancers

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype that is often associated with a poorer prognosis and does not respond to hormonal therapy. Increasing evidence highlights the exploitability of Annexin A1 (AnxA1), a calcium dependent protein, as a precision medicine for TNBC. To systematically summarize the role of AnxA1 and its associated mechanisms in TNBC, we performed data mining using three main databases: PubMed, Scopus, and Ovid/Medline. The papers retrieved were based on two different sets of key words such as Annexin A1 or Lipocortin 1 and Breast cancer or TNBC. A total of 388 articles were identified, with 210 chosen for comprehensive screening and 13 papers that met inclusion criteria were included. Current evidence from cell culture studies showed that AnxA1 expression is correlated with NF-kappa B, which promotes migration by activating ERK phosphorylation. AnxaA1 also activates TGF-beta signaling which upregulates MMP-9 and miR196a expression to enhance epithelial-mesenchymal transition and migratory capacity of TNBC cells. AnxA1 can steer the macrophage polarization toward the M2 phenotype to create a pro-tumor immune environment. Existing research suggests a potential role of AnxA1 in the metastasis and immune landscape of TNBC tumors. Preclinical and clinical experiments are warranted to investigate the feasibility and effectiveness of targeting AnxA1 in TNBC.

Automated summary

AnxA1 plays an important role in TNBC, being associated with cell migration, epithelial-mesenchymal transition, macrophage polarization, and tumor metastasis and immune landscape. Further experimental studies are needed to investigate the feasibility and effectiveness of targeting AnxA1 for the treatment of TNBC.