Magi3, or membrane associated guanylate kinase, WW and PDZ domain containing 3, is a significant gene involved in multiple biological processes. It has been linked to various pathways, such as the Wnt/β -catenin, PI3K/Akt, and is known to interact with key proteins like c-Myc, β -catenin, and PTEN. It plays a crucial role in regulating cell proliferation, apoptosis, and cell cycle progression, making it important for normal cellular function and disease prevention [1,2,3,4]. Genetic models, like KO/CKO mouse models, could potentially provide deeper insights into its functions.

In colorectal cancer, low levels of Magi3 are related to recurrence and poor prognosis. Magi3 acts as an E3 ubiquitin ligase to degrade c-Myc, inhibiting cell growth, promoting apoptosis, and enhancing chemosensitivity to fluoropyrimidine-based chemotherapy [1].

In glioma, the loss of Magi3 expression enhances cell proliferation via down-regulation of PTEN expression, activating the PI3K/Akt pathway, while its overexpression suppresses glioma cell proliferation, migration, and cell cycle progression by negatively regulating the Wnt/β -catenin signaling [2,4].

In cervical cancer, HPV18 E6 reduces Magi3 levels, activating the Wnt/β -catenin pathway and promoting cell migration and invasion [3].

In renal cell carcinoma, low Magi3 levels are a high-risk factor, and Magi3 enhances sensitivity to sunitinib by suppressing the MAS/ERK axis [5].

In conclusion, Magi3 functions as a regulator in multiple cellular processes and signaling pathways. Through model-based research, it has been revealed to play a significant role in various cancer types, including colorectal, glioma, cervical, and renal cell carcinoma. Understanding Magi3 can potentially offer new strategies for cancer treatment and prognosis prediction.