Evidence map›Paper›PMID 28783174›Full record

ArticleOncogene2017

Lysine-specific demethylase LSD1 regulates autophagy in neuroblastoma through SESN2-dependent pathway.

S Ambrosio, C D Saccà, S Amente, S Paladino, L Lania, B Majello

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 87 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  4. Review
  5. Article
  6. The Biological Role and Clinical Significance of BECLIN-1 in Cancer.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Histone demethylases in autophagy and inflammation.Cell communication and signaling : CCS · 2025
    Review
  11. Review
  12. Article
  13. Review
  14. Epigenetic regulation ofAutophagy · 2024
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
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 1 institution in 1 country.

S AmbrosioDivision of Genetics, Department of Biology, University of Naples, 'Federico II', Naples, Italy.
C D SaccàDivision of Genetics, Department of Biology, University of Naples, 'Federico II', Naples, Italy.
S AmenteDepartment of Molecular Medicine and Medical Biotechnologies, University of Naples, 'Federico II', Naples, Italy.
S PaladinoDepartment of Molecular Medicine and Medical Biotechnologies, University of Naples, 'Federico II', Naples, Italy.
L LaniaDepartment of Molecular Medicine and Medical Biotechnologies, University of Naples, 'Federico II', Naples, Italy.
B MajelloDivision of Genetics, Department of Biology, University of Naples, 'Federico II', Naples, Italy.
University of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a physiological process, important for recycling of macromolecules and maintenance of cellular homeostasis. Defective autophagy is associated with tumorigenesis and has a causative role in chemotherapy resistance in leukemia and in solid cancers. Here, we report that autophagy is regulated by the lysine-specific demethylase LSD1/KDM1A, an epigenetic marker whose overexpression is a feature of malignant neoplasia with an instrumental role in cancer development. In the present study, we determine that two different LSD1 inhibitors (TCP and SP2509) as well as selective ablation of LSD1 expression promote autophagy in neuroblastoma cells. At a mechanistic level, we show that LSD1 binds to the promoter region of Sestrin2 (SESN2), a critical regulator of mTORC1 activity. Pharmacological inhibition of LSD1 triggers SESN2 expression that hampers mTORC1 activity, leading to enhanced autophagy. SESN2 overexpression suffices to promote autophagy in neuroblastoma cells, while loss of SESN2 expression reduces autophagy induced by LSD1 inhibition. Our findings elucidate a mechanism whereby LSD1 controls autophagy in neuroblastoma cells through SESN2 transcription regulation, and we suggest that pharmacological targeting of LSD1 may have effective therapeutic relevance in the control of autophagy in neuroblastoma.

Indexed as

AutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell Line, TumorGene ExpressionGene Expression Regulation, NeoplasticHistone DemethylasesHumansKaplan-Meier EstimateMechanistic Target of Rapamycin Complex 1NeuroblastomaNuclear ProteinsProtein TransportSestrinsSignal TransductionBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsHistone DemethylasesKDM1A protein, humanMechanistic Target of Rapamycin Complex 1Nuclear ProteinsSESN2 protein, humanSestrinsTFEB protein, human

Identifiers

PMID28783174
PMCPMC5717079
OpenAlexW2744988474

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.