Back to Journals » Hypoxia » Volume 2

Complex role of HIF in cancer: the known, the unknown, and the unexpected

Authors Tiburcio P, Choi H, HuangLE

Received 22 March 2014

Accepted for publication 22 April 2014

Published 18 June 2014 Volume 2014:2 Pages 59—70


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

Patricia Denise Tiburcio,1,2 Hyunsung Choi,1 L Eric Huang1,2

1Department of Neurosurgery, Clinical Neurosciences Center, University of Utah, Salt Lake City, UT, USA; 2Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA

Abstract: Tumor hypoxia has long been recognized as a driving force of malignant progression and therapeutic resistance. The discovery of hypoxia-inducible transcription factors (HIFs) has greatly advanced our understanding of how cancer cells cope with hypoxic stress by maintaining bioenergetics through the stimulation of glycolysis. Until recently, however, it remained perplexing why proliferative cancer cells opt for aerobic glycolysis, an energy-inefficient process of glucose metabolism. Furthermore, the role of HIF in cancer has also become complex. In this review, we highlight recent groundbreaking findings in cancer metabolism, put forward plausible explanations to the complex role of HIF, and underscore remaining issues in cancer biology.

Keywords: cancer biology, hypoxia, metabolism, oncogenic signaling

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]