Evidence map›Paper›PMID 26872377›Full record

ArticleOncotarget2016

Crosstalk between RON and androgen receptor signaling in the development of castration resistant prostate cancer.

Izhar Batth, Huiyoung Yun, Suleman Hussain, Peng Meng, Pawel Osmulski, Tim Hui-Ming Huang, Roble Bedolla, Amanda Profit, Robert Reddick, Addanki Kumar

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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
1.6field-weighted citation impact, top 17% 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, 18 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

10 authors at 6 institutions in 1 country.

Izhar BatthDepartment of Urology, The University of Texas Health Science Center, San Antonio, TX, USA.
Huiyoung YunDepartment of Pharmacology, The University of Texas Health Science Center, San Antonio, TX, USA.
Suleman HussainDepartment of Pharmacology, The University of Texas Health Science Center, San Antonio, TX, USA.
Peng MengDepartment of Urology, The University of Texas Health Science Center, San Antonio, TX, USA.
Pawel OsmulskiDepartment of Molecular Medicine, The University of Texas Health Science Center, San Antonio, TX, USA.
Tim Hui-Ming HuangDepartment of Molecular Medicine, The University of Texas Health Science Center, San Antonio, TX, USA.
Roble BedollaDepartment of Urology, The University of Texas Health Science Center, San Antonio, TX, USA.
Amanda ProfitDepartment of Pathology, The University of Texas Health Science Center, San Antonio, TX, USA.
Robert ReddickDepartment of Pathology, The University of Texas Health Science Center, San Antonio, TX, USA.
Addanki KumarDepartment of Urology, The University of Texas Health Science Center, San Antonio, TX, USA.
The University of Texas Health Science Center at San Antonio · USThe University of Texas Health Science Center · USUrology San Antonio · USSouth Texas Veterans Health Care System · USTexas Oncology · USThe University of Texas Health Science Center at Houston · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Robin Jean Leach · 1991 to 2026
$59.1M
Oxidative stress and programmed death pathways: Cross talk in pancreatic cancerR01AT007448 · NCCIH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI KUMAR, ADDANKI PRATAP · 2012 to 2016
$1.6M
TARGETING FLIP FOR PROSTATE CANCER PREVENTIONR01CA135451 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI KUMAR, ADDANKI PRATAP · 2008 to 2012
$1.5M
Akt/CREB signaling: Target for prostate cancerI01BX000766 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI KUMAR, ADDANKI PRATAP · 2011 to 2013
–
BLRD VA I01 BX000766NCCIH NIH HHS R01 AT007448NCI NIH HHS P30 CA054174NCI NIH HHS R01 CA135451
6 · The paper itself

Abstract

Castrate-resistant prostate cancer (CRPC) is the fatal form of prostate cancer. Although reactivation of androgen receptor (AR) occurs following androgen deprivation, the precise mechanism involved is unclear. Here we show that the receptor tyrosine kinase, RON alters mechanical properties of cells to influence epithelial to mesenchymal transition and functions as a transcription factor to differentially regulate AR signaling. RON inhibits AR activation and subset of AR-regulated transcripts in androgen responsive LNCaP cells. However in C4-2B, a castrate-resistant sub-line of LNCaP and AR-negative androgen independent DU145 cells, RON activates subset of AR-regulated transcripts. Expression of AR in PC-3 cells leads to activation of RON under androgen deprivation but not under androgen proficient conditions implicating a role for RON in androgen independence. Consistently, RON expression is significantly elevated in castrate resistant prostate tumors. Taken together our results suggest that RON activation could aid in promoting androgen independence and that inhibition of RON in combination with AR antagonist(s) merits serious consideration as a therapeutic option during hormone deprivation therapy.

Indexed as

ApoptosisBiomarkers, TumorCell ProliferationHumansMalePrognosisProstatic Neoplasms, Castration-ResistantReceptor Protein-Tyrosine KinasesReceptors, AndrogenSignal TransductionTumor Cells, CulturedAR protein, humanBiomarkers, TumorReceptor Protein-Tyrosine KinasesReceptors, AndrogenRON proteinapoptosiscastrate resistant prostate cancerFLIPMST1RRON

Identifiers

PMID26872377
PMCPMC4924697
OpenAlexW2256449214

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.