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Mitochondrial fission regulator 2 (MTFR2) is a mitochondrial protein involved in the regulation of mitochondrial fission, maintenance of aerobic respiration, and cellular bioenergetics. It plays key roles in promoting mitochondrial fission and switching mitochondrial glucose metabolism from oxidative phosphorylation to aerobic glycolysis, especially in cancer cells[1][2][3]. MTFR2 is upregulated in several cancers—including breast cancer, lung adenocarcinoma, glioma, and oral squamous carcinoma—where it drives cell proliferation, migration, invasion, and epithelial-mesenchymal transition, primarily via the HIF1α/2α pathways and AKT/Cyclin D1 signaling pathways[1][2]. High expression of MTFR2 is associated with advanced tumor stage and poor prognosis in breast and lung cancer patients and correlates with immune cell infiltration, such as Th2 cells, in the tumor microenvironment[1][2]. These findings suggest MTFR2 could be a novel prognostic biomarker and an emerging therapeutic target, though no direct pharmacological modulators are currently available or clinically validated[1][2].
null (no approved drugs directly targeting MTFR2; no mechanism of drug action described in cited literature)
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