Anxa10, a member of the annexin family, is a membrane-bound calcium-dependent phospholipid-binding protein. Although its exact function remains unclear in some aspects, it is involved in multiple biological processes and disease-related pathways [1,2]. Mouse models with Anxa10-specific CreERT2 have been used to study human gastric cancer subtypes, highlighting its potential as a research model for in-vivo studies on gastric cancer [4].

In cancer research, knockdown of Anxa10 in colorectal cancer cells induced ferroptosis by inhibiting autophagy-mediated TFRC degradation, thus suppressing CRC progression [1]. In melanoma, Anxa10 knockout reduced cell migration and metastatic activity, and regulated the N-to E-cadherin switch through the ANXA10-PKD1-SMAD6 axis [2]. In hepatocellular carcinoma, Anxa10 up-regulation inhibited cell proliferation and migration [3]. In papillary thyroid carcinoma, Anxa10 knockdown inhibited cell proliferation, promoted apoptosis, and inactivated the MAPK/ERK signaling pathway by down-regulating TSG101 [7]. In bladder cancer, low Anxa10 expression was associated with shorter progression-free survival and disease aggressiveness [8]. In upper and lower urothelial carcinoma, Anxa10 expression was inversely associated with tumor stage, grade, and TP53 expression [5]. In esophageal squamous cell carcinoma, ANXA10 induced by interaction with tumor-associated macrophages promoted cell growth [6].

In conclusion, Anxa10 is involved in multiple biological functions, especially in various cancer-related processes. Gene knockout or knockdown experiments, including those in KO mouse models, have revealed its roles in tumor progression, metastasis, and ferroptosis. These findings contribute to understanding the mechanisms of diseases such as colorectal, melanoma, liver, thyroid, bladder, urothelial, and esophageal cancers, potentially providing new targets for therapeutic strategies.