Evidence map›Paper›PMID 24304514›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Resveratrol prevents rapamycin-induced upregulation of autophagy and selectively induces apoptosis in TSC2-deficient cells.

Anya Alayev, Yang Sun, Rose B Snyder, Sara Malka Berger, Jane J Yu, Marina K Holz

Open access · greenAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Novel treatment strategies for lymphangioleiomyomatosis: a narrative review.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
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  8. Article
  9. Review
  10. Article
  11. The paradox of autophagy in Tuberous Sclerosis Complex.Genetics and molecular biology · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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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 at 4 institutions in 1 country.

Anya AlayevDepartment of Biology; Stern College for Women of Yeshiva University; New York, NY USA.
Yang SunBrigham and Women's Hospital and Harvard Medical School; Boston, MA USA.
Rose B SnyderDepartment of Biology; Stern College for Women of Yeshiva University; New York, NY USA.
Sara Malka BergerDepartment of Biology; Stern College for Women of Yeshiva University; New York, NY USA.
Jane J YuBrigham and Women's Hospital and Harvard Medical School; Boston, MA USA.
Marina K HolzDepartment of Biology; Stern College for Women of Yeshiva University; New York, NY USA; Department of Molecular Pharmacology; Stern College for Women of Yeshiva University; New York, NY USA; Albert Einstein Cancer Center; Albert Einstein College of Medicine; Bronx, NY USA.
New York Proton Center · USYeshiva University · USBrigham and Women's Hospital · USHarvard University · US

Funding

Targeting the Estrogen Pathway for the Prevention and Treatment of LAMR01HL098216 · NHLBI · UNIVERSITY OF CINCINNATI · PI YU, JANE · 2010 to 2014
$2.1M
The role of the mTOR signaling pathway in ER-positive breast cancerR15CA151112 · NCI · YESHIVA UNIVERSITY · PI HOLZ, MARINA K · 2010 to 2013
$951k
NCI NIH HHS CA151112NCI NIH HHS R15 CA151112NHLBI NIH HHS HL098216NHLBI NIH HHS R01 HL098216
6 · The paper itself

Abstract

The mammalian/mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway is hyperactivated in a variety of cancers and disorders, including lymphangioleiomyomatosis (LAM) and tuberous sclerosis complex (TSC), which are characterized by mutations in tumor suppressors TSC1 or TSC2. The concern with the use of mTORC1 inhibitors, such as rapamycin or its analogs (rapalogs), is that they cause upregulation of autophagy and suppress the negative feedback loop to Akt, which promotes cell survival, causing the therapy to be only partially effective, and relapse occurs upon cessation of treatment. In this study, we investigate the use of rapamycin in combination with resveratrol, a naturally occurring polyphenol, in TSC2-deficient cells. We tested whether such combination would prevent rapamycin-induced upregulation of autophagy and shift the cell fate toward apoptosis. We found that this combination treatment blocked rapamycin-induced upregulation of autophagy and restored inhibition of Akt. Interestingly, the combination of rapamycin and resveratrol selectively promoted apoptosis of TSC2-deficient cells. Thus, the addition of resveratrol to rapamycin treatment may be a promising option for selective and targeted therapy for diseases with TSC loss and mTORC1 hyperactivation.

Indexed as

AnimalsAntibiotics, AntineoplasticAntineoplastic Agents, PhytogenicApoptosisAutophagyCells, CulturedDrug SynergismHumansLymphangioleiomyomatosisMechanistic Target of Rapamycin Complex 1MiceMultiprotein ComplexesProto-Oncogene Proteins c-aktResveratrolSignal TransductionSirolimusAntibiotics, AntineoplasticAntineoplastic Agents, PhytogenicMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProto-Oncogene Proteins c-aktResveratrolSirolimusStilbenesTOR Serine-Threonine KinasesTSC2 protein, humanTsc2 protein, mouseTuberous Sclerosis Complex 2 ProteinTumor Suppressor ProteinsapoptosisautophagyLAMmTORrapamycinresveratrolTSC

Identifiers

PMID24304514
PMCPMC3956533
OpenAlexW2009971408

What OpenQuestion holds

Textmetadata
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.