Annexin A2 in Tumorigenesis and Immune Response

What is it about?

Annexin A2 (ANXA2) is a calcium-dependent phospholipid-binding protein, and widely used as marker in a variety of tumors. The purpose of this review is to update the pathological effects of ANXA2 mainly from the following three aspects: 1) We updated and summarized the pathological effects of ANXA2-mediated multiple signalling pathways to promote EMT process, tumor cell invasion and metastasis as well as accelerate the thymic degeneration and tumor drug resistance. 2) The pathological effects of ANXA2 monomer or heterotetramer found at three different sites: at the cell membrane, in the cytoplasm and nucleus during the occurrence and development of tumors and immune response were updated in detail. 3) This review focused on the experimental findings by using both cell culture and mouse models utilized mostly genetic engineering, chemical inhibitors, and antibodies. These data indicate that ANXA2 reduction leads to the inhibition of invasion and metastasis in multiple tumor cells, bleeding complications in acute promyelocytic leukemia, retinal angiogenesis, autoimmunity response and tumor drug resistance.

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Why is it important?

Multiple animal and cell experiments demonstrated that ANXA2 or ANXA2 phosphorylated at Tyr-23 was overexpressed in some tumors and positively associated with poor disease prognosis. A successful therapeutic effect can be obtained by either knocking out or disrupting ANXA2 in some animal models and in vitro experiments where ANXA2 is overexpressed. Especially the studies of the mechanisms of acquired resistance to EGFR-TKIs targeting therapy in NSCLC suggested that inhibition of ANXA2 overexpression and phosphorylation was superior to only inhibiting one single EMT pathway. Therefore, ANXA2 may serve as a crucial therapeutic target for numerous malignancies and the immune host response.