Evidence map›Paper›PMID 35986103›Full record

ArticleOncogene2022

Neuropilin-2 promotes lineage plasticity and progression to neuroendocrine prostate cancer.

Jing Wang, Jingjing Li, Lijuan Yin, Tianjie Pu, Jing Wei, Varsha Karthikeyan, Tzu-Ping Lin, Allen C Gao, Boyang Jason Wu

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-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

12 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

9 authors at 5 institutions in 3 countries.

Jing Wang *Department of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA.
Jingjing Li *Department of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA.ORCID http://orcid.org/0000-0002-0661-5642
Lijuan YinUro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.
Tianjie PuDepartment of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA.
Jing WeiDepartment of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA.
Varsha KarthikeyanSummer Undergraduate Research Fellowship Program, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA.ORCID http://orcid.org/0000-0003-3196-8850
Tzu-Ping LinDepartment of Urology, Taipei Veterans General Hospital, Taipei, Taiwan, 11217, Republic of China.
Allen C GaoDepartment of Urologic Surgery, University of California Davis, Sacramento, CA, 95817, USA.ORCID http://orcid.org/0000-0002-5966-9038
Boyang Jason WuDepartment of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, 99202, USA. boyang.wu@wsu.edu.ORCID http://orcid.org/0000-0002-2823-3573
Washington State University Spokane · USCedars-Sinai Medical Center · USNational Yang Ming Chiao Tung University · TWOregon State University · USUniversity of California, Davis · US

Funding

MAOA and AR Reciprocal Crosstalk in Prostate CancerR37CA233658 · NCI · WASHINGTON STATE UNIVERSITY · PI WU, BOYANG · 2019 to 2025
$2.4M
NCI NIH HHS R37 CA233658
6 · The paper itself

Abstract

Neuroendocrine prostate cancer (NEPC), a lethal subset of prostate cancer, is characterized by loss of AR signaling and resulting resistance to AR-targeted therapy during neuroendocrine transdifferentiation, for which the molecular mechanisms remain unclear. Here, we report that neuropilin 2 (NRP2) is upregulated in both de novo and therapy-induced NEPC, which induces neuroendocrine markers, neuroendocrine cell morphology, and NEPC cell aggressive behavior. NRP2 silencing restricted NEPC tumor xenograft growth. Mechanistically, NRP2 engages in reciprocal crosstalk with AR, where NRP2 is transcriptionally inhibited by AR, and in turn suppresses AR signaling by downregulating the AR transcriptional program and confers resistance to enzalutamide. Moreover, NRP2 physically interacts with VEGFR2 through the intracellular SEA domain to activate STAT3 phosphorylation and subsequently SOX2, thus driving NEPC differentiation and growth. Collectively, these results characterize NRP2 as a driver of NEPC and suggest NRP2 as a potential therapeutic target in NEPC.

Indexed as

Carcinoma, NeuroendocrineProstatic NeoplasmsCell Line, TumorDisease ProgressionGene Expression Regulation, NeoplasticHumansMaleNeuropilin-2Neuropilin-2

Identifiers

PMID35986103
PMCPMC9464715
OpenAlexW4292316619

What OpenQuestion holds

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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.