Evidence map›Paper›PMID 25919885›Full record

ArticleAutophagy2015

Histone deacetylase inhibitors induce autophagy through FOXO1-dependent pathways.

Jianbin Zhang, Shukie Ng, Jigang Wang, Jing Zhou, Shi-Hao Tan, Naidi Yang, Qingsong Lin, Dajing Xia, Han-Ming Shen

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

118 citing papers in PubMed, 197 citations in OpenAlex.

  1. Review
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  7. Clinical progress and functional modalities of HDAC inhibitor-based combination therapies in cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Article
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  14. Review
  15. Mechanisms of HDACs in cancer development.Frontiers in immunology · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

58 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

9 authors at 4 institutions in 3 countries.

Jianbin Zhanga Department of Physiology ; Yong Loo Lin School of Medicine; National University of Singapore ; Singapore.
Shukie Ng
Jigang Wang
Jing Zhou
Shi-Hao Tan
Naidi Yang
Qingsong Lin
Dajing Xia
Han-Ming Shen
Yong In University · KRNational University of Singapore · SGGuangxi University of Chinese Medicine · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a catabolic process in response to starvation or other stress conditions to sustain cellular homeostasis. At present, histone deacetylase inhibitors (HDACIs) are known to induce autophagy in cells through inhibition of mechanistic target of rapamycin (MTOR) pathway. FOXO1, an important transcription factor regulated by AKT, is also known to play a role in autophagy induction. At present, the role of FOXO1 in the HDACIs-induced autophagy has not been reported. In this study, we first observed that HDACIs increased the expression of FOXO1 at the mRNA and protein level. Second, we found that FOXO1 transcriptional activity was enhanced by HDACIs, as evidenced by increased FOXO1 nuclear accumulation and transcriptional activity. Third, suppression of FOXO1 function by siRNA knockdown or by a chemical inhibitor markedly blocked HDACIs-induced autophagy. Moreover, we found that FOXO1-mediated autophagy is achieved via its transcriptional activation, leading to a dual effect on autophagy induction: (i) enhanced expression of autophagy-related (ATG) genes, and (ii) suppression of MTOR via transcription of the SESN3 (sestrin 3) gene. Finally, we found that inhibition of autophagy markedly enhanced HDACIs-mediated cell death, indicating that autophagy serves as an important cell survival mechanism. Taken together, our studies reveal a novel function of FOXO1 in HDACIs-mediated autophagy in human cancer cells and thus support the development of a novel therapeutic strategy by combining HDACIs and autophagy inhibitors in cancer therapy.

Indexed as

ApoptosisAutophagyCell SurvivalForkhead Box Protein O1Forkhead Transcription FactorsHistone Deacetylase InhibitorsHumansSignal TransductionTOR Serine-Threonine KinasesForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanHistone Deacetylase InhibitorsMTOR protein, humanTOR Serine-Threonine KinasesATG, autophagy-relatedautophagyBAF, bafilomycin A1cancercell deathCQ, chloroquineFOXO1FOXO, forkhead box OGFP, green fluorescent proteinhistone deacetylase inhibitorsMAP1LC3/LC3, microtubule-associated protein 1 light chain 3MEF, mouse embryonic fibroblastMTORMTOR, mechanistic target of rapamycinPI3K, phosphoinositide 3-kinaseSAHA, suberoylanilide hydroxamic acidsiRNA, short interfering RNATSA, trichostatin ATSC, tuberous sclerosis

Identifiers

PMID25919885
PMCPMC4502718
OpenAlexW1772484437

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.