Evidence map›Paper›PMID 27375022›Full record

ArticleOncogene2016

Neuroendocrine prostate cancer (NEPCa) increased the neighboring PCa chemoresistance via altering the PTHrP/p38/Hsp27/androgen receptor (AR)/p21 signals.

Y Cui, Y Sun, S Hu, J Luo, L Li, X Li, S Yeh, J Jin, C Chang

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 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 4 institutions in 3 countries.

Y CuiDepartment of Urology, Peking University/First Hospital, Beijing, China.
Y SunGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology and Radiation Oncology and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY, USA.
S HuDepartment of Urology, Peking University/First Hospital, Beijing, China.
J LuoGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology and Radiation Oncology and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY, USA.
L LiGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology and Radiation Oncology and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY, USA.
X LiDepartment of Urology, Peking University/First Hospital, Beijing, China.
S YehGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology and Radiation Oncology and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY, USA.
J JinDepartment of Urology, Peking University/First Hospital, Beijing, China.
C ChangGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology and Radiation Oncology and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY, USA.
Peking University · CNUniversity of Rochester Medical Center · USPeking University First Hospital · CNChina Medical University · TW

Funding

Non-AR mediated DHT-promoted Bladder Cancer initiation and progressionR01CA155477 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG · 2011 to 2015
$1.6M
Stromal AR Roles in Prostate Hyperplasia and CancerR01CA156700 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA155477NCI NIH HHS R01 CA156700
6 · The paper itself

Abstract

Prostatic neuroendocrine cells (NE) are an integral part of prostate cancer (PCa) and are associated with PCa progression. As the current androgen deprivation therapy with anti-androgens may promote the neuroendocrine PCa (NEPCa) development, and few therapies can effectively suppress NEPCa, understanding the impact of NEPCa on PCa progression may help us to develop better therapies to battle PCa. Here, we found NEPCa cells could increase the docetaxel resistance of their neighboring PCa cells. Mechanism dissection revealed that through secretion of PTHrP, NEPCa cells could alter the p38/MAPK/Hsp27 signals in their neighboring PCa cells that resulted in increased androgen receptor (AR) activity via promoting AR nuclear translocation. The consequences of increased AR function might then increase docetaxel resistance via increasing p21 expression. In vivo xenograft mice experiments also confirmed that NEPCa could increase the docetaxel resistance of neighboring PCa, and targeting this newly identified PTHrP/p38/Hsp27/AR/p21 signaling pathway with either p38 inhibitor (SB203580) or shPTHrP may result in improving/restoring the docetaxel sensitivity to better suppress PCa.

Indexed as

Drug Resistance, NeoplasmSignal TransductionAnimalsAntineoplastic AgentsCarcinoma, NeuroendocrineCell Line, TumorDisease Models, AnimalDocetaxelHSP27 Heat-Shock ProteinsHumansMalep38 Mitogen-Activated Protein KinasesProstatic NeoplasmsProtein Kinase InhibitorsReceptor, Parathyroid Hormone, Type 1Receptors, AndrogenAntineoplastic AgentsDocetaxelHSP27 Heat-Shock Proteinsp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsReceptor, Parathyroid Hormone, Type 1Receptors, AndrogenTaxoids

Identifiers

PMID27375022
PMCPMC5198573
OpenAlexW2468985637

What OpenQuestion holds

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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.