MTFR1, or mitochondrial fission regulator 1, is a nuclear gene encoding a mitochondrial protein crucial for regulating mitochondrial dynamics [6,7]. It is involved in processes like mitochondrial fission, fusion, and respiration, and plays a role in maintaining mitochondrial function and cellular antioxidant activity [6,7]. It may also participate in various signaling pathways related to cell survival, metabolism, and proliferation [1,2,3,4].

MTFR1 has been shown to be highly expressed in multiple cancers. In tongue squamous cell carcinoma, its knockdown inhibits TGFβ1-induced epithelial-mesenchymal transition (EMT), migration, and invasion [1]. In lung adenocarcinoma, overexpression promotes cancer progression, drug-resistance to cisplatin, and is related to the immune microenvironment; interfering with its expression inhibits cell proliferation, migration, invasion, and promotes cisplatin sensitivity [2]. In colon cancer, MTFR1 phosphorylation during glucose deprivation promotes mitochondrial fusion and cell survival [3]. In addition, in cardiomyocytes, knocking down Mtfr1 suppresses mitochondrial fission, apoptosis, and myocardial infarction [5].

In conclusion, MTFR1 is essential for regulating mitochondrial dynamics and function, and its dysregulation is associated with various diseases, especially cancers. Studies using gene-knockdown or knockout models in different cell types and animal models have revealed its role in promoting cancer progression, drug-resistance, and in cardiac diseases, highlighting its potential as a therapeutic target.