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Prieto-Domínguez N, Ordóñez R, Fernández A, et al. Modulation of Autophagy by Sorafenib: Effects on Treatment Response. Front Pharmacol. 2016;7:151doi: 10.3389/fphar.2016.00151.
Prieto-Domínguez, N., Ordóñez, R., Fernández, A., García-Palomo, A., Muntané, J., González-Gallego, J., & Mauriz, J. L. (2016). Modulation of Autophagy by Sorafenib: Effects on Treatment Response. Frontiers in pharmacology, 7151. https://doi.org/10.3389/fphar.2016.00151
Prieto-Domínguez, Nestor, et al. "Modulation of Autophagy by Sorafenib: Effects on Treatment Response." Frontiers in pharmacology vol. 7 (2016): 151. doi: https://doi.org/10.3389/fphar.2016.00151
Prieto-Domínguez N, Ordóñez R, Fernández A, García-Palomo A, Muntané J, González-Gallego J, Mauriz JL. Modulation of Autophagy by Sorafenib: Effects on Treatment Response. Front Pharmacol. 2016 Jun 08;7:151. doi: 10.3389/fphar.2016.00151. eCollection 2016. PMID: 27375485; PMCID: PMC4896953.
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Front Pharmacol. 2016 Jun 08;7:151. doi: 10.3389/fphar.2016.00151. eCollection 2016.

Modulation of Autophagy by Sorafenib: Effects on Treatment Response.

Frontiers in pharmacology

Nestor Prieto-Domínguez, Raquel Ordóñez, Anna Fernández, Andres García-Palomo, Jordi Muntané, Javier González-Gallego, José L Mauriz

Affiliations

  1. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd)León, Spain; Institute of Biomedicine (IBIOMED), University of LeónLeón, Spain.
  2. Service of Clinical Oncology, Complejo Asistencial Universitario de León (Hospital of León) León, Spain.
  3. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd)León, Spain; Department of General Surgery"Virgen del Rocío"-"Virgen Macarena" University Hospital/IBiS/CSIC/Universidad de Sevilla, Spain.

PMID: 27375485 PMCID: PMC4896953 DOI: 10.3389/fphar.2016.00151

Abstract

The multikinase inhibitor sorafenib is, at present, the only drug approved for the treatment of hepatocellular carcinoma (HCC), one of the most lethal types of cancer worldwide. However, the increase in the number of sorafenib tumor resistant cells reduces efficiency. A better knowledge of the intracellular mechanism of the drug leading to reduced cell survival could help to improve the benefits of sorafenib therapy. Autophagy is a bulk cellular degradation process activated in a broad range of stress situations, which allows cells to degrade misfolded proteins or dysfunctional organelles. This cellular route can induce survival or death, depending on cell status and media signals. Sorafenib, alone or in combination with other drugs is able to induce autophagy, but cell response to the drug depends on the complex integrative crosstalk of different intracellular signals. In cancerous cells, autophagy can be regulated by different cellular pathways (Akt-related mammalian target of rapamycin (mTOR) inhibition, 5' AMP-activated protein kinase (AMPK) induction, dissociation of B-cell lymphoma 2 (Bcl-2) family proteins from Beclin-1), or effects of some miRNAs. Inhibition of mTOR signaling by sorafenib and diminished interaction between Beclin-1 and myeloid cell leukemia 1 (Mcl-1) have been related to induction of autophagy in HCC. Furthermore, changes in some miRNAs, such as miR-30α, are able to modulate autophagy and modify sensitivity in sorafenib-resistant cells. However, although AMPK phosphorylation by sorafenib seems to play a role in the antiproliferative action of the drug, it does not relate with modulation of autophagy. In this review, we present an updated overview of the effects of sorafenib on autophagy and its related activation pathways, analyzing in detail the involvement of autophagy on sorafenib sensitivity and resistance.

Keywords: autophagy; cancer therapeutic; dug resistance; hepatocellular carcinoma; sorafenib

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