AnxA3

Annexin A3 (ANXA3) is a calcium-dependent phospholipid-binding member of the annexin family that participates in membrane-associated signaling and cellular regulatory processes, with particularly high expression reported in differentiated myeloid cells and neutrophils^[1][3]. Mechanistically, ANXA3 has been linked to pathways governing cell proliferation, migration, apoptosis, angiogenesis, and therapeutic response, including phosphatidylinositol-3 kinase/protein kinase B (PI3K/AKT), NF-κB, ERK, c-Jun, and hypoxia-inducible factor-1 (HIF-1) signaling networks^[2][4]. ANXA3 can promote vascular endothelial growth factor (VEGF) production through HIF-1 activation and has therefore been implicated in angiogenic regulation and tumor-associated vascular remodeling^[4]. In disease settings, dysregulated ANXA3 expression has been reported across multiple malignancies, including liver, lung, colorectal, gastric, breast, and prostate cancers, where it is associated with tumor progression, invasion, metastasis, angiogenesis, and resistance to anticancer therapies^[1][3]. Compared with related annexin family members, ANXA3 is distinguished by the presence of two major isoforms, a 36-kDa form and a 33-kDa form, which display cell-type-specific expression patterns and may exert distinct biological functions^[1][5]. Experimental studies indicate that the 33-kDa isoform contributes to hepatocarcinoma growth, metastasis, angiogenesis, and chemoresistance, highlighting the importance of isoform-specific investigation rather than analysis of total ANXA3 alone^[5]. For research applications, ANXA3 inhibition or knockdown is frequently used to evaluate mechanisms of tumor progression, therapeutic resistance, and pathway regulation in cellular and animal disease models^[1][3].

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