Evidence map›Paper›PMID 24752784›Full record

ArticleJournal of cellular physiology2014

Dependence of castration-resistant prostate cancer (CRPC) stem cells on CRPC-associated fibroblasts.

Helty Adisetiyo, Mengmeng Liang, Chun-Peng Liao, Joseph H Jeong, Michael B Cohen, Pradip Roy-Burman, Baruch Frenkel

Abstract readComparative Study
In one paragraph

Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

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  10. The Role of Nkx3.1 in Cancers and Stemness.International journal of stem cells · 2021
    Review
  11. Article
  12. Prevention of breast cancer by dietary polyphenols-role of cancer stem cells.Critical reviews in food science and nutrition · 2020
    Review
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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

7 authors at 3 institutions in 1 country.

Helty AdisetiyoBiochemistry and Molecular Biology, University of Southern California, Los Angeles, California; Institute for Genetic Medicine, University of Southern California, Los Angeles, California.
Mengmeng Liang
Chun-Peng Liao
Joseph H Jeong
Michael B Cohen
Pradip Roy-Burman
Baruch Frenkel
University of Southern California · USMedical College of Wisconsin · USUniversity of Utah · US

Funding

PATHOGENESIS OF HUMAN PROSTATE CARCINOMASR01CA059705 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ROY-BURMAN, PRADIP · 1993 to 2012
$7.3M
Sex Steroids and Runx Signaling in BoneR01DK071122 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI FRENKEL, BARUCH · 2005 to 2013
$2.5M
Bone matrix proteins in prostate cancer progressionR01CA113392 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ROY-BURMAN, PRADIP · 2005 to 2010
$1.6M
NCI NIH HHS R01 CA059705NCI NIH HHS R01CA059705NCI NIH HHS R01 CA113392NCI NIH HHS R01CA113392NIDDK NIH HHS R01 DK071122NIDDK NIH HHS R01DK71122
6 · The paper itself

Abstract

We previously established a role for cancer-associated fibroblasts (CAF) in enhancing the self-renewal and differentiation potentials of putative prostate cancer stem cells (CSC). Our published work focused on androgen-dependent prostate cancer (ADPC) using the conditional Pten deletion mouse model. Employing the same model, we now describe the interaction of CAF and CSC in castration-resistant prostate cancer (CRPC). CAF isolated from ADPC (ADPCAF) and from CRPC (CRPCAF) were compared in terms of their ability to support organoid formation and tumor initiation by CSC from CRPC (CRPCSC) in vitro and in vivo. CRPCSC formed spheroids in vitro and well-differentiated glandular structures under the renal capsules of recipient mice in vivo more effectively in the presence of CRPCAF compared to ADPCAF. Furthermore, whereas CSC with CAF from ADPC formed mostly well-differentiated tumors in our previous study, we now show that CRPCSC, when combined with CRPCAF (but not ADPCAF), can form aggressive, poorly-differentiated tumors. The potential of CRPCAF to support organoid/tumor formation by CRPCSC remained greater even when compared to 10-fold more ADPCAF, suggesting that paracrine factors produced specifically by CRPCAF preferentially potentiate the stemness and tumorigenic properties of the corresponding CSC. This apparently unique property of CRPCAF was notable when the CAF and CSC were grafted in either intact or castrated recipient mice. In both environments, CRPCAF induced in the epithelial compartment higher proliferative activity compared to ADPCAF, indicated by a higher Ki67 index. Factors released by CRPCAF to regulate CRPCSC may be targeted to develop novel therapeutic approaches to manage advanced prostate cancer.

Indexed as

Paracrine CommunicationAnimalsBiomarkers, TumorCastrationCell DifferentiationCell ProliferationFibroblastsMaleMiceMice, Inbred NODMice, KnockoutMice, SCIDNeoplastic Stem CellsProstatic Neoplasms, Castration-ResistantPTEN PhosphohydrolaseSignal TransductionBiomarkers, TumorPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID24752784
PMCPMC5774665
OpenAlexW1947290102

What OpenQuestion holds

Textmetadata
LicenceTDM
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.