Evidence map›Paper›PMID 19050678›Full record

ArticleAsian journal of andrology2009

Chimeric molecules facilitate the degradation of androgen receptors and repress the growth of LNCaP cells.

Yue-Qing Tang, Bang-Min Han, Xin-Quan Yao, Yan Hong, Yan Wang, Fu-Jun Zhao, Sheng-Qiang Yu, Xiao-Wen Sun, Shu-Jie Xia

Open access · goldAbstract read
In one paragraph

Article in Asian journal of andrology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. The androgen receptor-targeted proteolysis targeting chimera and other alternative therapeutic choices in overcoming the resistance to androgen deprivation treatment in prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  4. Overcoming Cancer Drug Resistance Utilizing PROTAC Technology.Frontiers in cell and developmental biology · 2022
    Review
  5. Review
  6. The PROTAC technology in drug development.Cell biochemistry and function · 2019
    Review
  7. Article
  8. Targeted protein knockdown using small molecule degraders.Current opinion in chemical biology · 2017
    Review
  9. Review
  10. Protacs for treatment of cancer.Pediatric research · 2010
    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

9 authors at 3 institutions in 1 country.

Yue-Qing TangDepartment of Urology, Shanghai First People's Hospital, Shanghai Jiao Tong University, Shanghai, China
Bang-Min Han
Xin-Quan Yao
Yan Hong
Yan Wang
Fu-Jun Zhao
Sheng-Qiang Yu
Xiao-Wen Sun
Shu-Jie Xia
Shanghai First People's Hospital · CNShanghai Jiao Tong University · CNWujiang District People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-translational degradation of protein plays an important role in cell life. We employed chimeric molecules (dihydrotestosterone-based proteolysis-targeting chimeric molecule [DHT-PROTAC]) to facilitate androgen receptor (AR) degradation via the ubiquitin-proteasome pathway (UPP) and to investigate the role of AR in cell proliferation and viability in androgen-sensitive prostate cancer cells. Western blot analysis and immunohistochemistry were applied to analyse AR levels in LNCaP cells after DHT-PROTAC treatment. Cell counting and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) cell viability assay were used to evaluate cell proliferation and viability after AR elimination in both LNCaP and PC-3 cells. AR was tagged for elimination via the UPP by DHT-PROTAC, and this could be blocked by proteasome inhibitors. Degradation of AR depended on DHT-PROTAC concentration, and either DHT or an ALAPYIP-(arg)(8) peptide could compete with DHT-PROTAC. Inhibition of cell proliferation and decreased viability were observed in LNCaP cells, but not in PC-3 or 786-O cells after DHT-PROTAC treatment. These data indicate that AR elimination is facilitated via the UPP by DHT-PROTAC, and that the growth of LNCaP cells is repressed after AR degradation.

Indexed as

Cell Line, TumorCell ProliferationCell SurvivalDihydrotestosteroneDose-Response Relationship, DrugHumansMaleProstatic NeoplasmsProteasome Endopeptidase ComplexReceptors, AndrogenRecombinant Fusion ProteinsSignal TransductionUbiquitinDihydrotestosteroneProteasome Endopeptidase ComplexReceptors, AndrogenRecombinant Fusion ProteinsUbiquitin

Identifiers

PMID19050678
PMCPMC3735208
OpenAlexW2150211787

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.