Among the major drivers are proteins involved in biosynthesis of heme intermediates (hydroxymethylbilane synthase (HMBS) and uroporphyrinogen decarboxylase (UROD)) and heme trafficking (FLVCR1). The only exception to heme overdrive in normal tissues is identified in preimplantation human embryos, where heme overdrive likely links to embryonic omnipotency. While heme overdrive is absent in diverse differentiated cells or somatic stem cells, it is present in hundreds of cancers, and is delineated in patient-derived tumor progenitor cells by single cell RNAseq. Three key characteristics define heme overdrive, i.e., cancer universality, cancer essentiality and cancer specificity. In this study, we report that all cancer cells employ imbalanced and dynamic heme metabolic pathways essential for their oncogenic growth and coined the term ‘heme overdrive’.
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