MTFR2, or mitochondrial fission regulator 2, is a gene that plays a crucial role in promoting mitochondrial fission. It is associated with various cellular pathways, including those related to metabolic reprogramming, such as the shift from oxidative phosphorylation to glycolysis. It has been implicated in the carcinogenesis and development of numerous cancers, highlighting its importance in understanding cancer biology [1,3,4,6,7].

In multiple types of cancer, including hepatocellular carcinoma (HCC), oral squamous carcinoma, lung adenocarcinoma, gastric cancer, breast cancer, and endometrial carcinoma, MTFR2 is upregulated and associated with poor prognosis. In HCC, MTFR2-dependent mitochondrial fission promotes cancer progression, and it can shape the immune microenvironment and accelerate HCC via metabolic reprogramming through the Akt signaling pathway [1,2,3]. In oral squamous carcinoma, it promotes proliferation, migration, and invasion by switching OXPHOS to glycolysis [4]. In lung adenocarcinoma, knockdown of MTFR2 inhibits cell proliferation, migration, and invasion via AKT-cyclin D1 signaling and EMT pathways [5]. In gastric cancer, its down-regulation inhibits cell proliferation, migration, and invasion both in vitro and in vivo [6]. In breast cancer, it promotes growth, migration, invasion, and tumour progression by switching glucose metabolism from OXPHS to glycolysis [7]. In endometrial carcinoma, it promotes cell proliferation and growth through the miR-132-3p/PI3K/Akt signaling pathway [8].

In conclusion, MTFR2 is a key regulator in promoting mitochondrial fission and is significantly involved in the progression of multiple cancers. The findings from various studies on MTFR2 in different cancer types using cell-based and in vivo models have provided valuable insights into its role in disease development, suggesting that MTFR2 could be a potential prognostic biomarker and therapeutic target for these cancers.