Oncogenic regulation of tumor metabolic reprogramming

Míriam Tarrado-Castellarnau, Pedro de Atauri and Marta Cascante _

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Oncotarget. 2016; 7:62726-62753. https://doi.org/10.18632/oncotarget.10911

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Míriam Tarrado-Castellarnau1, Pedro de Atauri1 and Marta Cascante1

1 Department of Biochemistry and Molecular Biomedicine, Universitat de Barcelona, Institute of Biomedicine of Universitat de Barcelona (IBUB) and CSIC-Associated Unit, Barcelona, Spain

Correspondence to:

Marta Cascante, email:

Keywords: metabolic reprogramming, MYC, HIF, PI3K, mTOR

Received: February 03, 2016 Accepted: June 29, 2016 Published: July 28, 2016


Development of malignancy is accompanied by a complete metabolic reprogramming closely related to the acquisition of most of cancer hallmarks. In fact, key oncogenic pathways converge to adapt the metabolism of carbohydrates, proteins, lipids and nucleic acids to the dynamic tumor microenvironment, conferring a selective advantage to cancer cells. Therefore, metabolic properties of tumor cells are significantly different from those of non-transformed cells. In addition, tumor metabolic reprogramming is linked to drug resistance in cancer treatment. Accordingly, metabolic adaptations are specific vulnerabilities that can be used in different therapeutic approaches for cancer therapy. In this review, we discuss the dysregulation of the main metabolic pathways that enable cell transformation and its association with oncogenic signaling pathways, focusing on the effects of c-MYC, hypoxia inducible factor 1 (HIF1), phosphoinositide-3-kinase (PI3K), and the mechanistic target of rapamycin (mTOR) on cancer cell metabolism. Elucidating these connections is of crucial importance to identify new targets and develop selective cancer treatments that improve response to therapy and overcome the emerging resistance to chemotherapeutics.

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