MYG1

MYG1 (Melanocyte Proliferation Gene 1), also known as C12orf10, Gamm1, and MYG, is a 3′-5′ RNA exonuclease with dual nuclear and mitochondrial localization, playing a critical role in mitochondrial function. MYG1 is encoded by a gene within the human genome, and its mechanism of action includes involvement in RNA processing and coordination of nuclear and mitochondrial translation programs, acting as a coordinator of nuclear-mitochondrial communication. The dual localization of MYG1 is essential for mitochondrial function and cellular respiration, processes that rely on its exonuclease activity.

MYG1 is involved in the regulation of multiple physiological and pathological processes. In tumor cells, MYG1 promotes glycolysis independently of its exonuclease activity. Studies have found that MYG1 is upregulated in colorectal cancer (CRC), and high expression of MYG1 accelerates glycolysis and CRC progression. Mechanistically, nuclear MYG1 recruits the HSP90/GSK3β complex to promote PKM2 phosphorylation, increasing its stability. PKM2 transcriptionally activates MYC and promotes MYC-mediated glycolysis. Conversely, c-Myc also upregulates MYG1 expression through transcription, driving CRC progression. Meanwhile, mitochondrial MYG1 inhibits oxidative phosphorylation and blocks the release of Cytc from mitochondria, suppressing apoptosis. Clinically, patients with KRAS mutations express high levels of MYG1, indicating high glycolytic levels and poor prognosis. Targeting MYG1 may disrupt the metabolic balance in colorectal cancer, making it a potential target for diagnosis and treatment of colorectal cancer.

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Recombinant Human UPF0160 protein MYG1, mitochondrial (C12orf10)