Hypoxia-inducible factors (HIFs) control cellular adaptation to oxygen deprivation. Cancer cells engage HIFs to sustain their growth in adverse conditions, thus promoting a cellular reprograming that includes metabolism, proliferation, survival and mobility. HIFs overexpression in human cancer biopsies correlates with high metastasis and mortality. A recent report has elucidated a novel mechanism for HIFs regulation in triple-negative breast cancer. Specifically, the basic helix-loop-helix (bHLH), Sharp-1, serves HIF1α to the proteasome and promotes its O 2-indendpendet degradation, counteracting HIF-mediated metastasis. These findings shed light on how HIFs are manipulated during cancer pathogenesis.

Amelio, I., Melino, G. (2012). The "Sharp" blade against HIF-mediated metastasis. CELL CYCLE, 11(24), 4530-4535 [10.4161/cc.22820].

The "Sharp" blade against HIF-mediated metastasis

Amelio, I;MELINO, GENNARO
2012-12-15

Abstract

Hypoxia-inducible factors (HIFs) control cellular adaptation to oxygen deprivation. Cancer cells engage HIFs to sustain their growth in adverse conditions, thus promoting a cellular reprograming that includes metabolism, proliferation, survival and mobility. HIFs overexpression in human cancer biopsies correlates with high metastasis and mortality. A recent report has elucidated a novel mechanism for HIFs regulation in triple-negative breast cancer. Specifically, the basic helix-loop-helix (bHLH), Sharp-1, serves HIF1α to the proteasome and promotes its O 2-indendpendet degradation, counteracting HIF-mediated metastasis. These findings shed light on how HIFs are manipulated during cancer pathogenesis.
15-dic-2012
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/11 - BIOLOGIA MOLECOLARE
English
Gene Expression Regulation, Neoplastic; Hypoxia-Inducible Factor 1; Animals; Humans; Neoplasm Metastasis; Breast Neoplasms; Models, Biological; Basic Helix-Loop-Helix Transcription Factors; Female
Amelio, I., Melino, G. (2012). The "Sharp" blade against HIF-mediated metastasis. CELL CYCLE, 11(24), 4530-4535 [10.4161/cc.22820].
Amelio, I; Melino, G
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/77877
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