Evidence map›Paper›PMID 27375485›Full record

ReviewFrontiers in pharmacology2016

Modulation of Autophagy by Sorafenib: Effects on Treatment Response.

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

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
10.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
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  7. Metabolic Reprogramming in Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2024
    Review
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8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Nestor Prieto-DomínguezCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd)León, Spain; Institute of Biomedicine (IBIOMED), University of LeónLeón, Spain.
Raquel OrdóñezCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd)León, Spain; Institute of Biomedicine (IBIOMED), University of LeónLeón, Spain.
Anna FernándezCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd)León, Spain; Institute of Biomedicine (IBIOMED), University of LeónLeón, Spain.
Andres García-PalomoService of Clinical Oncology, Complejo Asistencial Universitario de León (Hospital of León) León, Spain.
Jordi MuntanéCentro 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.
Javier González-GallegoCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd)León, Spain; Institute of Biomedicine (IBIOMED), University of LeónLeón, Spain.
José L MaurizCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd)León, Spain; Institute of Biomedicine (IBIOMED), University of LeónLeón, Spain.
Universidad de León · ESCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESHospital de León · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

autophagycancer therapeuticdug resistancehepatocellular carcinomasorafenib

Identifiers

PMID27375485
PMCPMC4896953
OpenAlexW2412783057

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.