Evidence map›Paper›PMID 25607466›Full record

ArticleAutophagy2015

TXNDC17 promotes paclitaxel resistance via inducing autophagy in ovarian cancer.

Song-Fa Zhang, Xin-Yu Wang, Zhi-Qin Fu, Qiao-Hua Peng, Jian-Yang Zhang, Feng Ye, Yun-Feng Fu, Cai-Yun Zhou, Wei-Guo Lu, Xiao-Dong Cheng and 1 more

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 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 168 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Autophagy in Ovarian Cancer, an Opportunity or an Additional Threat?International journal of molecular sciences · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Cancer chemoprevention: signaling pathways and strategic approaches.Signal transduction and targeted therapy · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

48 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

11 authors at 5 institutions in 2 countries.

Song-Fa Zhanga Women's Reproductive Health Laboratory of Zhejiang Province; Women's Hospital; School of Medicine ; Zhejiang University ; Hangzhou , China.
Xin-Yu Wang
Zhi-Qin Fu
Qiao-Hua Peng
Jian-Yang Zhang
Feng Ye
Yun-Feng Fu
Cai-Yun Zhou
Wei-Guo Lu
Xiao-Dong Cheng
Xing Xie
Zhejiang University · CNIndiana University School of MedicineWomen's Hospital · USWomen's Hospital, School of Medicine, Zhejiang University · CNHangzhou Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paclitaxel is recommended as a first-line chemotherapeutic agent against ovarian cancer, but drug resistance becomes a major limitation of its success clinically. The key molecule or mechanism associated with paclitaxel resistance in ovarian cancer still remains unclear. Here, we showed that TXNDC17 screened from 356 differentially expressed proteins by LC-MS/MS label-free quantitative proteomics was more highly expressed in paclitaxel-resistant ovarian cancer cells and tissues, and the high expression of TXNDC17 was associated with poorer prognostic factors and exhibited shortened survival in 157 ovarian cancer patients. Moreover, paclitaxel exposure induced upregulation of TXNDC17 and BECN1 expression, increase of autophagosome formation, and autophagic flux that conferred cytoprotection for ovarian cancer cells from paclitaxel. TXNDC17 inhibition by siRNA or enforced overexpression by a pcDNA3.1(+)-TXNDC17 plasmid correspondingly decreased or increased the autophagy response and paclitaxel resistance. Additionally, the downregulation of BECN1 by siRNA attenuated the activation of autophagy and cytoprotection from paclitaxel induced by TXNDC17 overexpression in ovarian cancer cells. Thus, our findings suggest that TXNDC17, through participation of BECN1, induces autophagy and consequently results in paclitaxel resistance in ovarian cancer. TXNDC17 may be a potential predictor or target in ovarian cancer therapeutics.

Indexed as

Antineoplastic Agents, PhytogenicApoptosisApoptosis Regulatory ProteinsAutophagyBeclin-1Cell Line, TumorCell SurvivalDrug Resistance, NeoplasmFemaleHumansMembrane ProteinsMicrotubule-Associated ProteinsOvarian NeoplasmsPaclitaxelThioredoxinsAntineoplastic Agents, PhytogenicApoptosis Regulatory ProteinsBeclin-1BECN1 protein, humanMembrane ProteinsMicrotubule-Associated ProteinsPaclitaxelThioredoxinsTXNDC17 protein, human95% CI, 95% confidence intervalALDOC, aldolase C, fructose-bisphosphateATG5, autophagy-related 5autophagyBafA1, bafilomycin A1BECN1BECN1, Beclin 1, autophagy-relatedCNN3, calponin 3, acidicDAPI, 4', 6-diamidino-2-phenylindoleFLNA, filamin A, αGenMAPP, gene microarray pathway profilerGO, gene ontologyHBSS, Hank's balanced salt solutionHR, hazard ratioKEGG, Kyoto encyclopedia of genes and genomeLC-MS/MS, liquid chromatography-mass spectrometry/ mass spectrometryMAP1LC3B/LC3B, microtubule-associated protein 1 light chain 3 βOS, overall survivalovarian cancerpaclitaxel resistancePFS, progression-free survivalPGAM1, phosphoglycerate mutase 1 (brain)siRNA, short interfering RNASQSTM1, sequestosome 1TNF, tumor necrosis factorTXNDC17TXNDC17, thioredoxin domain containing 17TXN, thioredoxinUTP23, small subunit (SSU) processome component, homolog (yeast)

Identifiers

PMID25607466
PMCPMC4502659
OpenAlexW1495956204

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.