Evidence map›Paper›PMID 25375374›Full record

ReviewCell death & disease2014

Regulation of autophagy by polyphenolic compounds as a potential therapeutic strategy for cancer.

N Hasima, B Ozpolat

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 2 pooled it
16.7field-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

123 citing papers in PubMed, 2 syntheses or guidelines pooled it, 256 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Article
  4. Review
  5. Article
  6. Article
  7. Gen inhibiting the Wnt/CaScientific reports · 2025
    Article
  8. Review
  9. Curcumin: a potential anti-photoaging agent.Frontiers in pharmacology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Resveratrol againstTropical medicine and infectious disease · 2023
    Article
  18. Article
  19. Review
  20. Review

63 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

2 authors at 1 institution in 1 country.

N Hasima1] Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 422, Houston, TX 77030, USA [2] Institute Science Biology, Faculty of Science, University of Malaya, Kuala Lumpur 50603, Malaysia [3] Center for Research in Biotechnology for Agriculture, University of Malaya, Kuala Lumpur 50603, Malaysia.
B Ozpolat1] Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 422, Houston, TX 77030, USA [2] Center for RNA Interference and Non-Coding RNAs - Red and Charline McCombs Institute for the Early Detection and Treatment of Cancer, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 422, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy, a lysosomal degradation pathway for cellular constituents and organelles, is an adaptive and essential process required for cellular homeostasis. Although autophagy functions as a survival mechanism in response to cellular stressors such as nutrient or growth factor deprivation, it can also lead to a non-apoptotic form of programmed cell death (PCD) called autophagy-induced cell death or autophagy-associated cell death (type II PCD). Current evidence suggests that cell death through autophagy can be induced as an alternative to apoptosis (type I PCD), with therapeutic purpose in cancer cells that are resistant to apoptosis. Thus, modulating autophagy is of great interest in cancer research and therapy. Natural polyphenolic compounds that are present in our diet, such as rottlerin, genistein, quercetin, curcumin, and resveratrol, can trigger type II PCD via various mechanisms through the canonical (Beclin-1 dependent) and non-canonical (Beclin-1 independent) routes of autophagy. The capacity of these compounds to provide a means of cancer cell death that enhances the effects of standard therapies should be taken into consideration for designing novel therapeutic strategies. This review focuses on the autophagy- and cell death-inducing effects of these polyphenolic compounds in cancer.

Indexed as

Gene Expression Regulation, NeoplasticAcetophenonesAntineoplastic Agents, PhytogenicApoptosisApoptosis Regulatory ProteinsAutophagyBeclin-1BenzopyransCell Line, TumorCurcuminGenisteinHumansMembrane ProteinsNeoplasmsPolyphenolsQuercetinAcetophenonesAntineoplastic Agents, PhytogenicApoptosis Regulatory ProteinsBeclin-1BECN1 protein, humanBenzopyransCurcuminGenisteinMembrane ProteinsPolyphenolsQuercetinResveratrolrottlerinStilbenes

Identifiers

PMID25375374
PMCPMC4260725
OpenAlexW1997184663

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.