Evidence map›Paper›PMID 21773856›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2011

Androgen receptor W741C and T877A mutations in AIDL cells, an androgen-independent subline of prostate cancer LNCaP cells.

Takashi Otsuka, Kazuhiro Iguchi, Kazuhiro Fukami, Kenichiro Ishii, Shigeyuki Usui, Yoshiki Sugimura, Kazuyuki Hirano

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.2field-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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Identification of Triptophenolide fromACS medicinal chemistry letters · 2016
    Article
  5. Article
  6. Article
  7. Quantitative synthesis of the association between the cytochrome P450 1A1 Ile462Val polymorphism and prostate cancer risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  8. Article
  9. Expression changes and regulation of AR and IGF-1 in PC3 prostate cancer cells treated with sexual hormones and flutamide.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
    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

7 authors at 2 institutions in 1 country.

Takashi OtsukaLaboratory of Pharmaceutics, Gifu Pharmaceutical University, 1-25-4 Daigaku-nishi, Gifu, 501-1196, Japan.
Kazuhiro Iguchi
Kazuhiro Fukami
Kenichiro Ishii
Shigeyuki Usui
Yoshiki Sugimura
Kazuyuki Hirano
Gifu Pharmaceutical University · JPMie University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The androgen-independent LNCaP (AIDL) cell line was generated by maintaining prostate cancer LNCaP cells in a hormone-deprived medium. Notably, synthetic androgen R1881-related gene response is attenuated in AIDL cells as compared to the parental LNCaP cells. The aim of this study was to clarify the mechanisms underlying androgen sensitivity in AIDL cells. We first examined the expression of androgen receptor (AR) and its co-regulators. However, no significant difference in mRNA expression was found between LNCaP and AIDL cells. Remarkably, AR protein levels were induced by R1881 and DHT in LNCaP cells, but not in AIDL cells. We next performed the cDNA sequencing to detect mutations in the AR gene. The T877A mutation was detected both in LNCaP and AIDL cells. Furthermore, AIDL cells harbored a missense substitution (TGG → TGT) in the AR gene, which caused a point mutation at codon 741 (W741C). Double T877A and W741C AR mutants have been previously reported to exhibit reduced androgen sensitivity. Hence, the low-androgen-sensitive responses of AIDL cells may be explained, at least in part, by AR gene mutations.

Indexed as

Mutation, MissensePoint MutationAndrogensBlotting, WesternCell Line, TumorDihydrotestosteroneDNA Mutational AnalysisGene Expression Regulation, NeoplasticHumansMaleMetriboloneProstatic NeoplasmsReceptors, AndrogenReverse Transcriptase Polymerase Chain ReactionAndrogensAR protein, humanDihydrotestosteroneMetriboloneReceptors, Androgen

Identifiers

PMID21773856
OpenAlexW2093382902

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.