Evidence map›Paper›PMID 33930758›Full record

ArticleNeoplasia (New York, N.Y.)2021

Synergistic effect of Chloroquine and Panobinostat in ovarian cancer through induction of DNA damage and inhibition of DNA repair.

María Ovejero-Sánchez, Rogelio González-Sarmiento, Ana Belén Herrero

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Autophagy in Ovarian Cancer, an Opportunity or an Additional Threat?International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Epigenetic Modulation of Estrogen Receptor Signaling in Ovarian Cancer.International journal of molecular sciences · 2024
    Review
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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

3 authors at 1 institution in 1 country.

María Ovejero-SánchezInstitute of Biomedical Research of Salamanca (IBSAL), Salamanca, Spain; Molecular Medicine Unit, Department of Medicine, University of Salamanca, Salamanca, Spain; Institute of Molecular and Cellular Biology of Cancer (IBMCC), University of Salamanca-CSIC, Salamanca, Spain.
Rogelio González-SarmientoInstitute of Biomedical Research of Salamanca (IBSAL), Salamanca, Spain; Molecular Medicine Unit, Department of Medicine, University of Salamanca, Salamanca, Spain; Institute of Molecular and Cellular Biology of Cancer (IBMCC), University of Salamanca-CSIC, Salamanca, Spain. Electronic address: gonzalez@usal.es.
Ana Belén HerreroInstitute of Biomedical Research of Salamanca (IBSAL), Salamanca, Spain; Molecular Medicine Unit, Department of Medicine, University of Salamanca, Salamanca, Spain; Institute of Molecular and Cellular Biology of Cancer (IBMCC), University of Salamanca-CSIC, Salamanca, Spain. Electronic address: anah@usal.es.
Universidad de Salamanca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer (OC) is the deadliest gynecologic malignancy, which is mainly due to late-stage diagnosis and chemotherapy resistance. Therefore, new and more effective treatments are urgently needed. The in vitro effects of Panobinostat (LBH), a histone deacetylase inhibitor that exerts pleiotropic antitumor effects but induces autophagy, in combination with Chloroquine (CQ), an autophagy inhibitor that avoid this cell survival mechanism, were evaluated in 4 OC cell lines. LBH and CQ inhibited ovarian cancer cell proliferation and induced apoptosis, and a strong synergistic effect was observed when combined. Deeping into their mechanisms of action we show that, in addition to autophagy modulation, treatment with CQ increased reactive oxygen species (ROS) causing DNA double strand breaks (DSBs), whereas LBH inhibited their repair by avoiding the correct recruitment of the recombinase Rad51 to DSBs. Interestingly, CQ-induced DSBs and cell death caused by CQ/LBH combination were largely abolished by the ROS scavenger N-Acetylcysteine, revealing the critical role of DSB generation in CQ/LBH-induced lethality. This role was also manifested by the synergy found when we combined CQ with Mirin, a well-known homologous recombination repair inhibitor. Altogether, our results provide a rationale for the clinical investigation of CQ/LBH combination in ovarian cancer.

Indexed as

Antineoplastic AgentsApoptosisAutophagyCell Cycle CheckpointsCell Line, TumorCell SurvivalChloroquineDNA Breaks, Double-StrandedDNA DamageDNA RepairDrug SynergismFemaleHumansOvarian NeoplasmsPanobinostatReactive Oxygen SpeciesAntineoplastic AgentsChloroquinePanobinostatReactive Oxygen SpeciesautophagyChloroquineDNA damage andrepairhomologous recombinationPanobinostatROS

Identifiers

PMID33930758
PMCPMC8100353
OpenAlexW3159734763

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.