The Role Of Hypoxia-Induced Autophagy In Cancer

Thu, 02/11/2010 - 13:20

Hypoxia inhibiting factors protect the cell from death. Autophagy proteins do the opposite. However, hypoxia-induced autophagy has been shown to have a role in cell survival by targeting only the organelles which are oxygen-demanding i.e. mitochondria. Although useful, the mechanism has been implicated in the development of tumours, therefore antibodies against the relevant proteins feature highly in the cancer research pages of our antibody catalogue.

Cell survival under hypoxic conditions is controlled by the HIF (hypoxia-inducible factor) family, complexes of transcriptional proteins which are normally dormant, but are activated by the reduction of intracellular oxygen tension. HIF proteins control a number of gene pathways which then work to restore homeostasis. Several of these proteins have shown to be active in forming cancerous tumours.

Western Blot: HIF-1 alpha Antibody Western Blot: HIF-1 alpha Antibody

Research using antibodies specific to the HIF-1 activation domains of C-TAD and N-TAD uncovered evidence about the dual role HIF-1 plays in hypoxia. HIF inhibiting factor FIH inhibits only the C-TAD domain. BNIP-3, a pro-autophagic gene, is expressed by the active N-TAD domain. However, the BNIP-3L gene, which shares a close link with BNIP-3, is expressed by both domains but inhibited by FIH.

Studies using the BNIP-3L antibody has shown inhibition is directly linked to the level of hypoxia. While this would seem to be beneficial, HIF is expressed at moderate levels of hypoxia, since if the DNA becomes damaged DNA-repair mechanisms come into play. Thus a hypoxia-induced cell-survival mechanism at critical hypoxic levels could encourage tumour growth. In fact, it has been shown that FIH expression was at critical levels in necrotic tumours.

We at Novus Biologicals continue to expand our antibody database to support this valuable work.

Novus Biologicals offers many HIF-1 reagents for your research needs including:


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