Evidence map›Paper›PMID 38474084›Full record

ArticleInternational journal of molecular sciences2024

Integrated Bioinformatics Analysis Identified ASNS and DDIT3 as the Therapeutic Target in Castrate-Resistant Prostate Cancer.

Ae Ryang Jung, Sun Shin, Mee Young Kim, U-Syn Ha, Sung-Hoo Hong, Ji Youl Lee, Sae Woong Kim, Yeun-Jun Chung, Yong Hyun Park

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026
    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

9 authors at 2 institutions in 1 country.

Ae Ryang JungDepartment of Urology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Sun ShinDepartment of Integrated Research Center for Genome Polymorphism, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Mee Young KimDepartment of Urology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
U-Syn HaDepartment of Urology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Sung-Hoo HongDepartment of Urology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Ji Youl LeeDepartment of Urology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.ORCID 0000-0001-6775-1157
Sae Woong KimDepartment of Urology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Yeun-Jun ChungDepartment of Integrated Research Center for Genome Polymorphism, The Catholic University of Korea, Seoul 06591, Republic of Korea.ORCID 0000-0002-6943-5948
Yong Hyun ParkDepartment of Urology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.ORCID 0000-0003-4860-6127
The Catholic University of Korea Seoul St. Mary's Hospital · KRCatholic University of Korea · KR

Funding

National Research Foundation of Korea 2022R1A2C2003513Seoul St. Mary's Hospital SC23eisi0844
6 · The paper itself

Abstract

Many studies have demonstrated the mechanisms of progression to castration-resistant prostate cancer (CRPC) and novel strategies for its treatment. Despite these advances, the molecular mechanisms underlying the progression to CRPC remain unclear, and currently, no effective treatments for CRPC are available. Here, we characterized the key genes involved in CRPC progression to gain insight into potential therapeutic targets. Bicalutamide-resistant prostate cancer cells derived from LNCaP were generated and named Bical R. RNA sequencing was used to identify differentially expressed genes (DEGs) between LNCaP and Bical R. In total, 631 DEGs (302 upregulated genes and 329 downregulated genes) were identified. The Cytohubba plug-in in Cytoscape was used to identify seven hub genes (

Indexed as

Prostatic Neoplasms, Castration-ResistantCarbon-Nitrogen Ligases with Glutamine as Amide-N-DonorCell Line, TumorComputational BiologyHumansMaleTranscription Factor CHOPTreatment OutcomeASNS protein, humanCarbon-Nitrogen Ligases with Glutamine as Amide-N-DonorDDIT3 protein, humanTranscription Factor CHOPbioinformaticscastration-resistant prostate cancergene expressionnovel key genesprostate cancerRNA-sequencing

Identifiers

PMID38474084
PMCPMC10932076
OpenAlexW4392295904

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.