Evidence map›Paper›PMID 27308421›Full record

ReviewMolecular & cellular oncology

Molecular mechanisms of mTOR regulation by stress.

Alexander Martin Heberle, Mirja Tamara Prentzell, Karen van Eunen, Barbara Marleen Bakker, Sushma Nagaraja Grellscheid, Kathrin Thedieck

Abstract readReview
In one paragraph

Review in Molecular & cellular oncology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
–field-weighted citation impact
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

60 citing papers in PubMed.

  1. Review
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  9. Maresin 1 modulates renal and cardiac lipid profiles in hypertensive rats.American journal of physiology. Renal physiology · 2025
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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

6 authors.

Alexander Martin HeberleDepartment of Pediatrics and Centre for Systems Biology of Energy Metabolism and Ageing; University of Groningen ; University Medical Center Groningen (UMCG); Groningen , The Netherlands.
Mirja Tamara PrentzellDepartment of Pediatrics and Centre for Systems Biology of Energy Metabolism and Ageing; University of Groningen; University Medical Center Groningen (UMCG); Groningen, The Netherlands; Faculty of Biology; Institute for Biology 3; Albert-Ludwigs-University Freiburg; Freiburg, Germany; Spemann Graduate School of Biology and Medicine (SGBM); University of Freiburg; Freiburg, Germany.
Karen van EunenDepartment of Pediatrics and Centre for Systems Biology of Energy Metabolism and Ageing; University of Groningen; University Medical Center Groningen (UMCG); Groningen, The Netherlands; Top Institute Food and Nutrition; Wageningen, The Netherlands.
Barbara Marleen BakkerDepartment of Pediatrics and Centre for Systems Biology of Energy Metabolism and Ageing; University of Groningen ; University Medical Center Groningen (UMCG); Groningen , The Netherlands.
Sushma Nagaraja GrellscheidSchool of Biological and Biomedical Sciences; Durham University ; Durham , UK.
Kathrin ThedieckDepartment of Pediatrics and Centre for Systems Biology of Energy Metabolism and Ageing; University of Groningen; University Medical Center Groningen (UMCG); Groningen, The Netherlands; Faculty of Biology; Institute for Biology 3; Albert-Ludwigs-University Freiburg; Freiburg, Germany; School of Medicine and Health Sciences; Carl von Ossietzky University Oldenburg; Oldenburg, Germany; BIOSS Centre for Biological Signaling Studies; Albert-Ludwigs-University Freiburg; Freiburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumors are prime examples of cell growth in unfavorable environments that elicit cellular stress. The high metabolic demand and insufficient vascularization of tumors cause a deficiency of oxygen and nutrients. Oncogenic mutations map to signaling events via mammalian target of rapamycin (mTOR), metabolic pathways, and mitochondrial function. These alterations have been linked with cellular stresses, in particular endoplasmic reticulum (ER) stress, hypoxia, and oxidative stress. Yet tumors survive these challenges and acquire highly energy-demanding traits, such as overgrowth and invasiveness. In this review we focus on stresses that occur in cancer cells and discuss them in the context of mTOR signaling. Of note, many tumor traits require mTOR complex 1 (mTORC1) activity, but mTORC1 hyperactivation eventually sensitizes cells to apoptosis. Thus, mTORC1 activity needs to be balanced in cancer cells. We provide an overview of the mechanisms contributing to mTOR regulation by stress and suggest a model wherein stress granules function as guardians of mTORC1 signaling, allowing cancer cells to escape stress-induced cell death.

Indexed as

apoptosisbalancecancercell deathER stresshyperactivationhypoxiamammalian target of rapamycinmTORC1mTORC2oxidative stressRNA granulesstress granulessurvival

Identifiers

PMID27308421
PMCPMC4904989

What OpenQuestion holds

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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.