By M. Celeste Simon
Hypoxia, outlined as decreased oxygen stress, is a standard physiological phenomenon in either general embryonic improvement and malignancy development. even if serious hypoxia is mostly poisonous for either general tissue and tumors, neoplastic cells progressively adapt to lengthy hypoxia even though extra genetic and genomic adjustments with a internet end result that hypoxia promotes tumor development and healing resistance. Hypoxia promotes melanoma development through regulating a number of elements of melanoma biology, together with radiotherapy resistance, metabolism, angiogenesis and invasion/migration
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Extra info for Diverse Effects of Hypoxia on Tumor Progression (Current Topics in Microbiology and Immunology, Vol. 345)
Nat Rev Cancer 8(12):967 975 Bolos V, Blanco M et al (2009) Notch signalling in cancer stem cells. Clin Transl Oncol 11(1):11 19 Bonnet D, Dick JE (1997) Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat Med 3(7):730 737 Calabrese C, Poppleton H et al (2007) A perivascular niche for brain tumor stem cells. Cancer Cell 11(1):69 82 Carroll VA, Ashcroft M (2006) Role of hypoxia inducible factor (HIF) 1alpha versus HIF 2alpha in the regulation of HIF target genes in response to hypoxia, insulin like growth factor I, or loss of von Hippel Lindau function: implications for targeting the HIF pathway.
Cancer stem cells (CSCs), also known as cancer initiating cells or tumor propagation cells, are neoplastic cells that could selfrenewal, differentiate as well as initiate tumor growth in vivo. Cancer stem cells are believed to be the key drivers in tumor growth and therapy resistance. Hypoxia has been shown to help maintain multiple normal stem cell population but its roles in cancer stem cells were largely unknown. Our group and other researchers recently identified that hypoxia is also a critical microenvironmental factor in regulating cancer stem cells’ self-renewal, partially by enhancing the activity of stem cell factors like Oct4, c-Myc and Nanog.
Several other transcription factors are also activated by hypoxia: cyclic-AMP response element binding (CREB) protein, the activator protein-1 (AP1), the nuclear factor kb (NF-kb), and the early growth response-1 protein (Egr-1).