Evidence map›Paper›PMID 28386843›Full record

ArticleMolecular and cellular biochemistry2017

Differential expression of AP-1 transcription factors in human prostate LNCaP and PC-3 cells: role of Fra-1 in transition to CRPC status.

K Kavya, M Naveen Kumar, Rajeshwari H Patil, Shubha M Hegde, K M Kiran Kumar, Rashmi Nagesh, R L Babu, Govindarajan T Ramesh, S Chidananda Sharma

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Article in Molecular and cellular biochemistry, 2017. 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
1.8field-weighted citation impact, top 14% 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, 17 citations in OpenAlex.

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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 2 institutions in 2 countries.

K KavyaDepartment of Microbiology and Biotechnology, Bangalore University, Jnana Bharathi, Bengaluru, 560 056, Karnataka, India.
M Naveen KumarDepartment of Microbiology and Biotechnology, Bangalore University, Jnana Bharathi, Bengaluru, 560 056, Karnataka, India.
Rajeshwari H PatilDepartment of Microbiology and Biotechnology, Bangalore University, Jnana Bharathi, Bengaluru, 560 056, Karnataka, India.
Shubha M HegdeDepartment of Microbiology and Biotechnology, Bangalore University, Jnana Bharathi, Bengaluru, 560 056, Karnataka, India.
K M Kiran KumarDepartment of Microbiology and Biotechnology, Bangalore University, Jnana Bharathi, Bengaluru, 560 056, Karnataka, India.
Rashmi NageshDepartment of Microbiology and Biotechnology, Bangalore University, Jnana Bharathi, Bengaluru, 560 056, Karnataka, India.
R L BabuDepartment of Bioinformatics and Biotechnology, Karnataka State Women's University, Jnanashakthi Campus, Vijayapura, 586 108, Karnataka, India.
Govindarajan T RameshDepartment of Biology and Center for Biotechnology and Biomedical Sciences, Norfolk State University, Norfolk, VA, USA.
S Chidananda SharmaDepartment of Microbiology and Biotechnology, Bangalore University, Jnana Bharathi, Bengaluru, 560 056, Karnataka, India. sharma@bub.ernet.in.
Bangalore University · INNorfolk State University · US

Funding

Department of Science and Technology-Promotion of University Research and Scientific Excellence (DST-PURSE) [SR/59/Z-23/2010/38(c)]University Grant Commission-Centre with Potential for Excellence in Particular Area (UGC-CPEPA) [8-2/2008(NS/PE)]
6 · The paper itself

Abstract

Androgen receptor (AR) signaling axis plays a vital role in the development of prostate and critical in the progression of prostate cancer. Androgen withdrawal initially regresses tumors but eventually develops into aggressive castration-resistant prostate cancer (CRPC). Activator Protein-1 (AP-1) transcription factors are most likely to be associated with malignant transformation in prostate cancer. Hence, to determine the implication of AR and AP-1 in promoting the transition of prostate cancer to the androgen-independent state, we used AR-positive LNCaP and AR-negative PC-3 cells as an in vitro model system. The effect of dihydrotestosterone or anti-androgen bicalutamide on the cell proliferation and viability was assessed by MTT assay. Expression studies on AR, marker genes-PSA, TMPRSS2, and different AP-1 factors were analyzed by semi-quantitative RT-PCR and expressions of AR and Fra-1 proteins were analyzed by Western blotting. Dihydrotestosterone induced the cell proliferation in LNCaP with no effect on PC-3 cells. Bicalutamide decreased the viability of both LNCaP and PC-3 cells. Dihydrotestosterone induced the expression of AR, PSA, c-Jun, and Fra-1 in LNCaP cells, and it was c-Jun and c-Fos in case of PC-3 cells, while bicalutamide decreased their expression. In addition, constitutive activation and non-regulation of Fra-1 by bicalutamide in PC-3 cells suggested that Fra-1, probably a key component, involved in transition of aggressive androgen-independent PC-3 cells with poor prognosis.

Indexed as

Gene Expression Regulation, NeoplasticCell Line, TumorFos-Related Antigen 1HumansMaleProstatic Neoplasms, Castration-ResistantProto-Oncogene Proteins c-fosTranscription Factor AP-1Fos-Related Antigen 1Proto-Oncogene Proteins c-fosTranscription Factor AP-1Androgen receptorBicalutamideCRPCDihydrotestosteroneRT-PCRWestern blot

Identifiers

PMID28386843
OpenAlexW2604442472

What OpenQuestion holds

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Registered trials

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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.