Evidence map›Paper›PMID 42026685›Full record

ArticleJournal of experimental & clinical cancer research : CR2026

Ferrodoxin 1 (FDX1) drives paclitaxel resistance in ovarian cancer via copper metabolism and ULK1/ATG13-mediated autophagy: overcome by pH/ROS-responsive PPD/PDP@si-FDX1 nanomicelles.

Yangmei Gong, Zhizhi Deng, Jie Wu, Yi Hu

Abstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. 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

4 authors.

Yangmei GongThe First Affiliated Hospital, Center for a combination of Obstetrics and Gynecology & Reproductive medicine, Henyang Medical School, University of South China, No. 69, Chuanshan Avenue, Hengyang, 421001, Hunan Province, China.
Zhizhi DengThe First Affiliated Hospital, Center for a combination of Obstetrics and Gynecology & Reproductive medicine, Henyang Medical School, University of South China, No. 69, Chuanshan Avenue, Hengyang, 421001, Hunan Province, China.
Jie WuThe First Affiliated Hospital, Center for a combination of Obstetrics and Gynecology & Reproductive medicine, Henyang Medical School, University of South China, No. 69, Chuanshan Avenue, Hengyang, 421001, Hunan Province, China.
Yi HuThe First Affiliated Hospital, Center for a combination of Obstetrics and Gynecology & Reproductive medicine, Henyang Medical School, University of South China, No. 69, Chuanshan Avenue, Hengyang, 421001, Hunan Province, China. 2018011528@usc.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOvarian cancer (OC) is often characterized by poor prognosis due to paclitaxel (TAX) resistance, with ferredoxin 1 (FDX1) emerging as a key mediator of copper metabolism. The present study aimed to elucidate the role of FDX1 in TAX resistance and to evaluate the efficacy of pH/reactive oxygen species (ROS)-responsive nanomicelles (PPD/PDP@si-FDX1) in reversing this resistance.

methodsTAX-resistant A2780 and SKOV3 cells were established by gradient exposure, and FDX1 expression was assessed using Western blotting. FDX1 was either overexpressed or silenced, and resistance was evaluated using CCK-8, clonogenic, scratch, and Transwell assays. Autophagic activity was examined through Western blotting, immunofluorescence, and transmission electron microscopy. Mechanistic validation involved the ULK1 activator BL-918 and the copper chelator TTM. PPD/PDP@si-FDX1 nanomicelles were prepared via self-assembly, with structural and responsive characteristics analyzed by transmission electron microscopy (TEM), dynamic light scattering (DLS), and drug release profiling. Tumor penetration and in vivo antitumor efficacy were examined using multicellular spheroids and subcutaneous xenograft models.

resultsFDX1 overexpression elevated intracellular copper, activated the ULK1/ATG13 autophagic axis, and enhanced TAX resistance; silencing FDX1 reversed these effects. Copper chelators or ULK1 inhibition phenocopied FDX1 silencing. PPD/PDP@si-FDX1 demonstrated pH/ROS-responsive tumor accumulation and enhanced si-FDX1 delivery. In vivo, it significantly suppressed tumor growth and restored TAX sensitivity, outperforming free si-FDX1.

conclusionFDX1 drives TAX resistance via copper-dependent ULK1/ATG13 activation; PPD/PDP@si-FDX1 nanomicelles effectively reverse resistance, offering a promising strategy for OC therapy.

Indexed as

Autophagy-Related Protein-1 HomologCopperDrug Resistance, NeoplasmFerredoxinsOvarian NeoplasmsPaclitaxelAnimalsAutophagyCell Line, TumorFemaleHumansHydrogen-Ion ConcentrationMiceMicellesReactive Oxygen SpeciesXenograft Model Antitumor AssaysAutophagy-Related Protein-1 HomologCopperFerredoxinsMicellesPaclitaxelReactive Oxygen SpeciesAutophagyAutophagy related 13CuproptosisFerredoxin 1Ovarian cancerPaclitaxel resistancePH/Reactive oxygen Species-Responsive nanomicellesUnc-51 like autophagy activating kinase 1

Identifiers

PMID42026685
PMCPMC13104215

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.