In general, tumor hypoxia induces angiogenesis for growth and dissemination of tumor cells. Now increasing evidence suggesting that, hypoxia may play a critical role in the differentiation of cancer stem cells.
What is the molecular mechanism underlining in these events?
Chronic or cycling hypoxia within solid tumor promotes inflammation and increases infiltration by myeloid cells (monocytes and macrophages). This infiltration of immune cells and their interactions with cancer epithelial cells, including stem cells provides advantage. See recent paper: http://www.ncbi.nlm.nih.gov/pubmed/25266422
Brain. 04/2010; 133(Pt 4):983-95. DOI: 10.1093/brain/awq042
This might help..
In this context, the central role is played by hypoxia inducible transcription factors (HIFs). Under normal oxygen tension (normoxia), HIF prolyl-hydroxylases catalyze hydroxylation of alpha-subunits of hypoxia inducible factors (HIFs) that leads to their rapid proteasomal degradation. Under hypoxic conditions, HIF alpha subunits are not hydroxylated and HIFs are stabilized. HIFs then induce expression of genes involved in self-renewal and maintenance of stem cells in undifferentiated state (OCT4, NANOG, SOX2...). HIF-1 target genes also modulate angiogenesis by stimulation of proliferation and migration of endothelial cells.
I know that my response comes in late ... but who knows?
Here attached are interesting articles (reviews).
Best regards
Robert
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