亚甲基四氢叶酸还原酶2 (Methylenetetrahydrofolate dehydrogenase 2, MTHFD2)是一种参与叶酸代谢的四甲基叶酸脱氢酶,主要位于线粒体内,在一碳代谢过程中催化亚甲基四氢叶酸成甲酰基四氢叶酸。MTHFD2在恶性肿瘤组织中表达上调,在正常...亚甲基四氢叶酸还原酶2 (Methylenetetrahydrofolate dehydrogenase 2, MTHFD2)是一种参与叶酸代谢的四甲基叶酸脱氢酶,主要位于线粒体内,在一碳代谢过程中催化亚甲基四氢叶酸成甲酰基四氢叶酸。MTHFD2在恶性肿瘤组织中表达上调,在正常组织中几乎不表达,在肿瘤代谢重编程中发挥重要作用,通过AKT、JAK/STAT等信号通路调控代谢,影响细胞一碳代谢、有氧糖酵解,以适应快速增值的细胞所需要的物质,多数证据都表明其与肿瘤的发生、预后有着密切的关系,并将其作为预后标志物或潜在的治疗靶点。目前MTHFD2在人类恶性肿瘤中的代谢作用机制尚未明确,未来深入研究MTHFD2在肿瘤代谢重编程与信号通路的关系及其作为肿瘤治疗靶标的作用,可为恶性肿瘤的治疗提供新决策。Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) is an enzyme involved in folate metabolism, primarily located in the mitochondria. It catalyzes the conversion of methylenetetrahydrofolate to formyltetrahydrofolate during one-carbon metabolism. MTHFD2 is upregulated in malignant tumors and is almost not expressed in normal tissues, playing a significant role in tumor metabolic reprogramming. It regulates metabolism through signaling pathways such as AKT and JAK/STAT, affecting cellular one-carbon metabolism and aerobic glycolysis to accommodate the needs of rapidly proliferating cells. Most evidence suggests a close relationship between MTHFD2 expression and tumor development and prognosis, making it a potential prognostic marker or therapeutic target. Currently, the mechanisms of MTHFD2’s metabolic roles in human malignancies are not well understood. Future in-depth studies on the relationship between MTHFD2 in tumor metabolic reprogramming and signaling pathways, and its role as a therapeutic target, could provide new decisions for the treatment of malignant tumors.展开更多
文摘亚甲基四氢叶酸还原酶2 (Methylenetetrahydrofolate dehydrogenase 2, MTHFD2)是一种参与叶酸代谢的四甲基叶酸脱氢酶,主要位于线粒体内,在一碳代谢过程中催化亚甲基四氢叶酸成甲酰基四氢叶酸。MTHFD2在恶性肿瘤组织中表达上调,在正常组织中几乎不表达,在肿瘤代谢重编程中发挥重要作用,通过AKT、JAK/STAT等信号通路调控代谢,影响细胞一碳代谢、有氧糖酵解,以适应快速增值的细胞所需要的物质,多数证据都表明其与肿瘤的发生、预后有着密切的关系,并将其作为预后标志物或潜在的治疗靶点。目前MTHFD2在人类恶性肿瘤中的代谢作用机制尚未明确,未来深入研究MTHFD2在肿瘤代谢重编程与信号通路的关系及其作为肿瘤治疗靶标的作用,可为恶性肿瘤的治疗提供新决策。Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) is an enzyme involved in folate metabolism, primarily located in the mitochondria. It catalyzes the conversion of methylenetetrahydrofolate to formyltetrahydrofolate during one-carbon metabolism. MTHFD2 is upregulated in malignant tumors and is almost not expressed in normal tissues, playing a significant role in tumor metabolic reprogramming. It regulates metabolism through signaling pathways such as AKT and JAK/STAT, affecting cellular one-carbon metabolism and aerobic glycolysis to accommodate the needs of rapidly proliferating cells. Most evidence suggests a close relationship between MTHFD2 expression and tumor development and prognosis, making it a potential prognostic marker or therapeutic target. Currently, the mechanisms of MTHFD2’s metabolic roles in human malignancies are not well understood. Future in-depth studies on the relationship between MTHFD2 in tumor metabolic reprogramming and signaling pathways, and its role as a therapeutic target, could provide new decisions for the treatment of malignant tumors.
