Evidence map›Paper›PMID 29050220›Full record

ArticleOncotarget2017

Characterization of a novel androgen receptor (AR) coregulator RIPK1 and related chemicals that suppress AR-mediated prostate cancer growth via peptide and chemical screening.

Cheng-Lung Hsu, Jai-Shin Liu, Ting-Wei Lin, Ying-Hsu Chang, Yung-Chia Kuo, An-Chi Lin, Huei-Ju Ting, See-Tong Pang, Li-Yu Lee, Wen-Lung Ma and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Steroid receptor/coactivator binding inhibitors: An update.Molecular and cellular endocrinology · 2019
    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

12 authors at 5 institutions in 1 country.

Cheng-Lung HsuDivision of Hematology-Oncology, Departments of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 333, Taiwan.
Jai-Shin LiuInstitute of Bioinformatics and Structural Biology, National Tsing Hua University, Hsinchu 300, Taiwan.
Ting-Wei LinDepartment of Chemistry, National Tsing-Hua University, Hsinchu 300, Taiwan.
Ying-Hsu ChangDivision of Urology, Department of Surgery, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 333, Taiwan.
Yung-Chia KuoDivision of Hematology-Oncology, Departments of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 333, Taiwan.
An-Chi LinDivision of Hematology-Oncology, Departments of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 333, Taiwan.
Huei-Ju TingDepartment of Biological Science and Technology, National University of Tainan, Tainan 700, Taiwan.
See-Tong PangDivision of Urology, Department of Surgery, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 333, Taiwan.
Li-Yu LeeDepartment of Pathology, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 333, Taiwan.
Wen-Lung MaSex Hormone Research Center, China Medical University Hospital, Taichung 104, Taiwan.
Chun-Cheng LinDepartment of Chemistry, National Tsing-Hua University, Hsinchu 300, Taiwan.
Wen-Guey WuInstitute of Bioinformatics and Structural Biology, National Tsing Hua University, Hsinchu 300, Taiwan.
National Tsing Hua University · TWChang Gung Memorial Hospital · TWChang Gung University · TWChina Medical University Hospital · TWNational University of Tainan · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Using bicalutamide-androgen receptor (AR) DNA binding domain-ligand binding domain as bait, we observed enrichment of FxxFY motif-containing peptides. Protein database searches revealed the presence of receptor-interacting protein kinase 1 (RIPK1) harboring one FxxFY motif. RIPK1 interacted directly with AR and suppressed AR transactivation in a dose-dependent manner. Domain mapping experiments showed that the FxxFY motif in RIPK1 is critical for interactions with AR and the death domain of RIPK1 plays a crucial role in its inhibitory effect on transactivation. In terms of tissue expression, RIPK1 levels were markedly higher in benign prostate hyperplasia and non-cancerous tissue regions relative to the tumor area. With the aid of computer modeling for screening of chemicals targeting activation function 2 (AF-2) of AR, we identified oxadiazole derivatives as good candidates and subsequently generated a small library of these compounds. A number of candidates could effectively suppress AR transactivation and AR-related functions

Indexed as

androgen receptorFxxLFoxadiazoleprostate cancerRIPK1

Identifiers

PMID29050220
PMCPMC5642495
OpenAlexW2613027230

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.