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1.
  • Canesin, Giacomo, et al. (författare)
  • Scavenging of Labile Heme by Hemopexin Is a Key Checkpoint in Cancer Growth and Metastases
  • 2020
  • Ingår i: Cell Reports. - : Elsevier BV. - 2211-1247. ; 32:12
  • Tidskriftsartikel (refereegranskat)abstract
    • Canesin et al. describe a role and mechanism for labile heme as a key player in regulating gene expression to promote carcinogenesis via binding to G-quadruplex in the c-MYC promoter. Hemopexin, a heme scavenger, may be used as a strategy to block progression of cancer.
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2.
  • Hedblom, Andreas, et al. (författare)
  • Heme detoxification by heme oxygenase-1 reinstates proliferative and immune balances upon genotoxic tissue injury
  • 2019
  • Ingår i: Cell Death and Disease. - : Nature Publishing Group. - 2041-4889. ; 10
  • Tidskriftsartikel (refereegranskat)abstract
    • Phenotypic changes of myeloid cells are critical to the regulation of premature aging, development of cancer, and responses to infection. Heme metabolism has a fundamental role in the regulation of myeloid cell function and activity. Here, we show that deletion of heme oxygenase-1 (HO-1), an enzyme that removes heme, results in an impaired DNA damage response (DDR), reduced cell proliferation, and increased cellular senescence. We detected increased levels of p16INK4a, H2AXγ, and senescence-associated-β-galactosidase (SA-β-Gal) in cells and tissues isolated from HO-1-deficient mice. Importantly, deficiency of HO-1 in residential macrophages in chimeric mice results in elevated DNA damage and senescence upon radiation-induced injury. Mechanistically, we found that mammalian target of rapamycin (mTOR)/S6 protein signaling is critical for heme and HO-1-regulated phenotype of macrophages. Collectively, our data indicate that HO-1, by detoxifying heme, blocks p16INK4a expression in macrophages, preventing DNA damage and cellular senescence.
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