Evidence map›Paper›PMID 34759344›Full record

ArticleOncogene2022

Targeting KDM4A-AS1 represses AR/AR-Vs deubiquitination and enhances enzalutamide response in CRPC.

Boya Zhang, Mingpeng Zhang, Yanjie Yang, Qi Li, Jianpeng Yu, Shimiao Zhu, Yuanjie Niu, Zhiqun Shang

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Role of Circular RNAs in Prostate Cancer.Current medicinal chemistry · 2024
    Review
  5. Article
  6. Article
  7. The roles of FLOT1 in human diseases (Review).Molecular medicine reports · 2023
    Review
  8. Review
  9. Article
  10. The crosstalk between ubiquitination and endocrine therapy.Journal of molecular medicine (Berlin, Germany) · 2023
    Review
  11. Post-transcriptional modification of mCell death & disease · 2023
    Article
  12. Targeting epigenetic regulators to overcome drug resistance in cancers.Signal transduction and targeted therapy · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Natural antisense transcripts as drug targets.Frontiers in molecular biosciences · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Boya Zhang *Tianjin Institute of Urology, the Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Mingpeng Zhang *Tianjin Institute of Urology, the Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Yanjie YangTianjin Institute of Urology, the Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Qi LiTianjin Institute of Urology, the Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Jianpeng YuTianjin Institute of Urology, the Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Shimiao ZhuTianjin Institute of Urology, the Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Yuanjie NiuTianjin Institute of Urology, the Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Zhiqun ShangTianjin Institute of Urology, the Second Hospital of Tianjin Medical University, Tianjin, 300211, China. zhiqun_shang@tmu.edu.cn.ORCID http://orcid.org/0000-0001-8263-707X
Second Hospital of Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Castration-resistant prostate cancer (CRPC) is a highly malignant type of advanced cancer resistant to androgen deprivation therapy. One of the important mechanisms for the development of CRPC is the persistent imbalanced regulation of AR and AR splice variants (AR/AR-Vs). In this study, we reported KDM4A-AS1, a recently discovered lncRNA, as a tumor promoter that was significantly increased in CRPC cell lines and cancer tissues. Depletion of KDM4A-AS1 significantly reduced cell viability, proliferation, migration in vitro, and tumor growth in vivo. We found that by binding to the NTD domain, KDM4A-AS1 enhances the stability of USP14-AR/AR-Vs complex, and promoted AR/AR-Vs deubiquitination to protect it from MDM2-mediated ubiquitin-proteasome degradation. Moreover, KDM4A-AS1 was found to enhance CRPC drug resistance to enzalutamide by repressing AR/AR-Vs degradation; antisense oligonucleotide drugs targeting KDM4A-AS1 significantly reduced the growth of tumors with enzalutamide resistance. Taken together, our results indicated that KDM4A-AS1 played an important role in the progression of CRPC and enzalutamide resistance by regulating AR/AR-Vs deubiquitination; targeting KDM4A-AS1 has broad clinical application potential.

Indexed as

AgedAnimalsBenzamidesCell Line, TumorHumansJumonji Domain-Containing Histone DemethylasesMaleMiceNitrilesPhenylthiohydantoinProstatic Neoplasms, Castration-ResistantBenzamidesenzalutamideJumonji Domain-Containing Histone DemethylasesKDM4A protein, humanNitrilesPhenylthiohydantoin

Identifiers

PMID34759344
PMCPMC8755543
OpenAlexW3212209145

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.