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Int. J. Mol. Sci. 2017, 18(9), 1854; doi:10.3390/ijms18091854

Targeting Tumor Adaption to Chronic Hypoxia: Implications for Drug Resistance, and How It Can Be Overcome

Graduate School of Analytical Science and Technology (GRAST), Chungnam National University, Daejeon 34134, Korea
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Received: 21 July 2017 / Revised: 21 August 2017 / Accepted: 22 August 2017 / Published: 25 August 2017
(This article belongs to the Special Issue Adaptation to Chronic Hypoxia: The Last Word Has Not yet Been Said)
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Abstract

The rapid and uncontrolled proliferation of tumors limits the availability of oxygen and nutrients supplied from the tumor vasculature, thus exposing them to low oxygen environments. Thus, diminished oxygen availability, or hypoxia, is the most common microenvironment feature of nearly all solid tumors. All living cells have the ability to sense changes in oxygen tension and adapt to this stress to preserve survival. Likewise, cancer cells adapt to chronic hypoxic stress via several mechanisms, including promotion of angiogenic factor production, metabolic shift to consume less oxygen, and reduction of apoptotic potential. Adaptation of tumor cells to hypoxia is believed to be the main driver for selection of more invasive and therapy-resistant cancer phenotypes. In this review, we discuss molecular mechanisms by which tumor cells adapt to hypoxia, with a specific focus on hypoxia-inducible factor (HIF) transcription factor. We further discuss the current understandings on hypoxia-mediated drug resistance and strategies to overcome it. View Full-Text
Keywords: chronic hypoxia; cancer; tumor; HIF-1α; drug resistance chronic hypoxia; cancer; tumor; HIF-1α; drug resistance
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Kim, J.-Y.; Lee, J.-Y. Targeting Tumor Adaption to Chronic Hypoxia: Implications for Drug Resistance, and How It Can Be Overcome. Int. J. Mol. Sci. 2017, 18, 1854.

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