Evidence map›Paper›PMID 39676352›Full record

ArticleMolecular cancer therapeutics2025

All-trans Retinoic Acid Sensitizes Epithelial Ovarian Cancer to PARP Inhibition after Exposure to Cisplatin.

Bingjie Mei, Junyang Li, Dengfeng Wang, Lu Feng, Jianming Huang, Guonan Zhang

Abstract read
In one paragraph

Article in Molecular cancer therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

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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

2 citing papers in PubMed.

  1. Article
  2. Review
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.

Bingjie Mei *Department of Gynecological Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu, China.ORCID 0009-0004-2103-4813
Junyang Li *Department of Gynecological Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu, China.ORCID 0000-0003-0089-6962
Dengfeng WangDepartment of Gynecological Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu, China.ORCID 0000-0002-1832-1270
Lu FengDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, China.ORCID 0009-0006-0080-5054
Jianming HuangBiochemistry and Molecular Biology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu, China.ORCID 0000-0002-6307-4977
Guonan ZhangDepartment of Gynecological Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu, China.ORCID 0000-0002-2228-9197

Funding

Kanghua Foundation for the Development of Traditional Chinese and Western Medicine Le Fund KH-2020-LJJ-07Scientific Research Foundation of Department of Science and Technology of Sichuan, China 2019YFS0036Scientific Research Foundation of Department of Science and Technology of Sichuan, China 23NSFSC1143
6 · The paper itself

Abstract

Epithelial ovarian cancer (EOC) is the most lethal of gynecologic malignancies. The standard-of-care treatment for EOC is platinum-based chemotherapy such as cisplatin (CDDP). Notably, platinum-based chemotherapy induces resistance of EOC to PARP inhibition. However, therapeutic approaches targeting PARP inhibitor (PARPi) resistance remain to be explored. In this study, we show that all-trans retinoic acid (ATRA) reduces PARPi resistance-associated EOC cells induced by CDDP treatment. Clinically applicable ATRA suppressed the outgrowth of CDDP-treated EOC cells both in vitro and in vivo. Moreover, a CDDP treatment followed by niraparib maintenance therapy in combination with ATRA improved the survival of EOC-bearing mice. These phenotypes correlated with the PARPi-resistant EOC signature, which consists of elevated expression of aldehyde dehydrogenase 1 family member A1, nicotinamide phosphoribosyltransferase, PARP1, and checkpoint kinase 1, as well as elevated NAD+ level-mediated high activity of aldehyde dehydrogenase 1 family member A1 and PARP1. Mechanistically, ATRA downregulates the expression of these genes and level of intracellular NAD+. Our results suggest that ATRA in conjunction with PARPi represents a promising maintenance therapeutic strategy for EOC.

Indexed as

Carcinoma, Ovarian EpithelialCisplatinOvarian NeoplasmsPoly(ADP-ribose) Polymerase InhibitorsTretinoinAnimalsCell Line, TumorDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansMiceXenograft Model Antitumor AssaysCisplatinPoly(ADP-ribose) Polymerase InhibitorsTretinoin

Identifiers

PMID39676352
PMCPMC11876957

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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.