Evidence map›Paper›PMID 25500540›Full record

ArticleOncogene2015

The role of TXNDC5 in castration-resistant prostate cancer-involvement of androgen receptor signaling pathway.

L Wang, G Song, X Chang, W Tan, J Pan, X Zhu, Z Liu, M Qi, J Yu, B Han

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Thioredoxin Domain Containing 5 (TXNDC5): Friend or Foe?Current issues in molecular biology · 2024
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. The role and mechanism of TXNDC5 in diseases.European journal of medical research · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

10 authors at 6 institutions in 2 countries.

L WangDepartment of Pathology, Shandong University Medical School, Jinan, China.
G SongInstitute of Basic Medicine, Shandong Academy of Medical Sciences, Jinan, China.
X ChangMedical Research Center of Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
W TanDepartment of Pathology, Shandong University Medical School, Jinan, China.
J PanResearch Center for Medicinal Biotechnology, Key Laboratory for Rare & Uncommon Diseases of Shandong Province, Shandong Academy of Medicinal Sciences, Jinan, China.
X ZhuShandong institute of medicine and health informations, Jinan, China.
Z LiuDepartment of Pathology, Shandong University Medical School, Jinan, China.
M QiDepartment of Pathology, Shandong University Medical School, Jinan, China.
J YuDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
B HanDepartment of Pathology, Shandong University Medical School, Jinan, China.
Shandong University · CNNorthwestern University · USQilu Hospital of Shandong University · CNShandong Academy of Pharmaceutical Sciences · CNShandong First Medical University · CNShandong Provincial QianFoShan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Castration-resistant prostate cancer (CRPC) continues to be a major clinical problem and the mechanisms behind it remain unclear. Thioredoxin domain-containing protein 5 (TXNDC5) is involved in protein folding and chaperone activity, and its overexpression has been reported in multiple malignancies. In the current study, we demonstrated that TXNDC5 is up-regulated following long-term androgen-deprivation treatment (ADT) and is highly overexpressed in CRPC tumors compared with hormone-naive prostate cancer (PCa) cases. Functionally, in vitro and in vivo studies demonstrated that TXNDC5 overexpression promotes the growth of both androgen-dependent and castration-resistant PCa xenografts. Mechanistically, TXNDC5 directly interacts with the AR protein to increase its stability and thus enhances its transcriptional activity. TXDNC5-mediated CRPC growth can be fully abolished by AR inhibition, suggesting TXDNC5 up-regulation as an escape pathway for aberrant AR re-activation and CRPC growth in the milieu of low androgen. Indeed, we found that TXNDC5 is increased by ADT-induced hypoxia through HIF-1α in an miR-200b-dependent manner. Overall, we defined an important role of TXNDC5 in CRPC and further investigations are needed to screen TXNDC5 antagonists as a novel therapeutic approaches to treat PCa patients with CRPC.

Indexed as

AndrogensAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMicroRNAsProstatic Neoplasms, Castration-ResistantProtein Disulfide-IsomerasesReceptors, AndrogenSignal TransductionAndrogensHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN200 microRNA, humanProtein Disulfide-IsomerasesReceptors, AndrogenTXNDC5 protein, human

Identifiers

PMID25500540
OpenAlexW2064960387

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.