Anxa3-flox Mouse

Anxa3, short for Annexin A3, is a component of the annexin family. It has been implicated in various cellular processes and signaling pathways. For instance, it can activate the AKT-GSK3β-β-catenin pathway, and is associated with processes like cell cycle progression, DNA replication, and ferroptosis regulation. It is also involved in the immune response, as seen in sepsis, and has implications in multiple disease conditions, making it a gene of significant biological importance [1-5].

In laryngeal squamous cell carcinoma, ANXA3-rich exosomes derived from tumor-associated macrophages promote lymphatic metastasis by inhibiting ferroptosis in cancer cells through an ATF2-CHAC1 axis [1]. In cervical cancer, knockdown of ANXA3 inhibits cell cycle progression and increases chemosensitivity to cisplatin, suggesting its role in cell proliferation and chemoresistance [2]. In colon cancer, ANXA3 expression is upregulated by hypoxia-inducible factor 1-alpha (HIF-1α) and contributes to tumor growth [3]. In ischemic stroke, ANXA3 may be a pyroptosis-related gene marker, and its silencing alleviates pyroptosis-related factor expression [4]. In intracranial aneurysm, ANXA3 silencing rescues vascular smooth muscle cell function by inhibiting the phosphorylation and activation of the JNK signaling pathway [5]. In lung cancer, knockdown of ANXA3 inhibits the resistance of lung cancer cells to oxaliplatin [6].

In conclusion, Anxa3 plays diverse and crucial roles in multiple biological processes and disease conditions. Studies using gene-knockdown or knockout models, though not always involving traditional KO/CKO mouse models in the references provided, have revealed its significance in cancer progression, chemoresistance, and in non-cancer diseases such as sepsis and ischemic stroke. Understanding Anxa3 provides insights into disease mechanisms and potential therapeutic targets.