Evidence map›Paper›PMID 38336745›Full record

ArticleNature communications2024

Androgen deprivation induces double-null prostate cancer via aberrant nuclear export and ribosomal biogenesis through HGF and Wnt activation.

Won Kyung Kim, Alyssa J Buckley, Dong-Hoon Lee, Alex Hiroto, Christian H Nenninger, Adam W Olson, Jinhui Wang, Zhuo Li, Rajeev Vikram, Yao Mawulikplimi Adzavon and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
10.9field-weighted citation impact, top 1% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  14. Therapeutic targeting of exportin-1 beyond nuclear export.Trends in pharmacological sciences · 2025
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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

16 authors at 4 institutions in 1 country.

Won Kyung Kim *Department of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Alyssa J Buckley *Department of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Dong-Hoon LeeDepartment of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Alex HirotoDepartment of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Christian H NenningerDepartment of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Adam W OlsonDepartment of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.ORCID 0000-0003-3118-0393
Jinhui WangIntegrative Genomics Core, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Zhuo LiElectronic Microscopy Core, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Rajeev VikramDepartment of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Yao Mawulikplimi AdzavonDepartment of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Tak-Yu YauDepartment of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Yigang BaoDepartment of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Michael KahnDepartment of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA.
Joseph GeradtsDepartment of Pathology and Laboratory Medicine, Brody School of Medicine, East Carolina University, Greenville, USA.
Guang-Qian XiaoDepartment of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0003-2111-5897
Zijie SunDepartment of Cancer Biology and Molecular Medicine, Cancer Center and Beckman Research Institute, City of Hope, Duarte, CA, USA. zjsun@coh.org.ORCID 0000-0002-6787-6272
City of Hope · USCity Of Hope National Medical Center · USEast Carolina University · USUniversity of Southern California · US

Funding

Roles of the androgen receptor and its co-regulators in prostate tumorigenesisR01CA070297 · NCI · STANFORD UNIVERSITY · PI SUN, ZIJIE · 2003 to 2025
$5.0M
DNA repair gene mutations and prostate cancerR01CA233664 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI SHEN, BINGHUI, SUN, ZIJIE · 2020 to 2024
$3.4M
Wnt responsive stem cells in the prostateR01DK104941 · NIDDK · STANFORD UNIVERSITY · PI SUN, ZIJIE · 2015 to 2024
$3.0M
A New Mechanism for Castration Resistant Prostate CancerR01CA166894 · NCI · STANFORD UNIVERSITY · PI SUN, ZIJIE · 2015 to 2018
$1.2M
Aberrant Activation of Androgen Signaling Pathways in African American Prostate CancerR01CA288392 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SUN, ZIJIE · 2024 to 2025
$1.1M
NCI NIH HHS R01 CA070297NCI NIH HHS R01 CA166894NCI NIH HHS R01 CA233664NCI NIH HHS R01 CA288392NIDDK NIH HHS R01 DK104941
6 · The paper itself

Abstract

Androgen deprivation therapy (ADT) targeting androgen/androgen receptor (AR)- signaling pathways is the main therapy for advanced prostate cancer (PCa). However, ADT eventually fails in most patients who consequently develop castration-resistant prostate cancer (CRPC). While more potent AR antagonists and blockers for androgen synthesis were developed to improve clinical outcomes, they also show to induce more diverse CRPC phenotypes. Specifically, the AR- and neuroendocrine-null PCa, DNPC, occurs in abiraterone and enzalutamide-treated patients. Here, we uncover that current ADT induces aberrant HGF/MET signaling activation that further elevates Wnt/β-catenin signaling in human DNPC samples. Co-activation of HGF/MET and Wnt/β-catenin axes in mouse prostates induces DNPC-like lesions. Single-cell RNA sequencing analyses identify increased expression and activity of XPO1 and ribosomal proteins in mouse DNPC-like cells. Elevated expression of XPO1 and ribosomal proteins is also identified in clinical DNPC specimens. Inhibition of XPO1 and ribosomal pathways represses DNPC growth in both in vivo and ex vivo conditions, evidencing future therapeutic targets.

Indexed as

AndrogensProstatic Neoplasms, Castration-ResistantActive Transport, Cell NucleusAndrogen AntagonistsAnimalsbeta CateninCell Line, TumorHepatocyte Growth FactorHumansMaleMiceReceptors, AndrogenRibosomal ProteinsWnt Signaling PathwayAndrogen AntagonistsAndrogensbeta CateninHepatocyte Growth FactorHGF protein, humanReceptors, AndrogenRibosomal Proteins

Identifiers

PMID38336745
PMCPMC10858246
OpenAlexW4391682254

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.