Evidence map›Paper›PMID 35455981›Full record

ArticleCells2022

MicroRNA-like snoRNA-Derived RNAs (sdRNAs) Promote Castration-Resistant Prostate Cancer.

Alexander B Coley, Ashlyn N Stahly, Mohan V Kasukurthi, Addison A Barchie, Sam B Hutcheson, Dominika Houserova, Yulong Huang, Brianna C Watters, Valeria M King, Meghan A Dean and 15 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  7. Selective remodeling of snoRNA and sdRNA biology in glioblastoma.Frontiers in cell and developmental biology · 2026
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  14. SnoRNAs: The promising targets for anti-tumor therapy.Journal of pharmaceutical analysis · 2024
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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

25 authors at 4 institutions in 1 country.

Alexander B ColeyDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Ashlyn N StahlyMedical Scientist Training Program, University of Colorado School of Medicine, Aurora, CO 80045, USA.
Mohan V KasukurthiSchool of Computing, University of South Alabama, Mobile, AL 36608, USA.
Addison A BarchieDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Sam B HutchesonDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Dominika HouserovaDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Yulong HuangDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Brianna C WattersDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Valeria M KingDepartment of Biology, University of South Alabama, Mobile, AL 36608, USA.
Meghan A DeanDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Justin T RobertsDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Jeffrey D DeMeisDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Krisha V AminDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Cameron H McInnisDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Noel L GodangDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Ryan M WrightDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
David F HaiderDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Neha B PirachaDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Cana L BrownDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Zohaib M IjazDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.
Shengyu LiSchool of Computing, University of South Alabama, Mobile, AL 36608, USA.
Yaguang XiDepartment of Genetics, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Oliver G McDonaldDepartment of Pathology, Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL 33146, USA.
Jingshan HuangSchool of Computing, University of South Alabama, Mobile, AL 36608, USA.
Glen M BorchertDepartment of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36608, USA.ORCID 0000-0002-6182-7154
University of South Alabama · USLouisiana State University Health Sciences Center New Orleans · USUniversity of Colorado Denver · USUniversity of Miami · US

Funding

Investigate interactive roles of environmental, behavioral and genetic factors on racial disparities in breast cancer outcomesR01CA260698 · NCI · UNIVERSITY OF GEORGIA · PI XI, YAGUANG · 2021 to 2025
$2.0M
NCI NIH HHS R01 CA260698
6 · The paper itself

Abstract

We have identified 38 specifically excised, differentially expressed snoRNA fragments (sdRNAs) in TCGA prostate cancer (PCa) patient samples as compared to normal prostate controls. SnoRNA-derived fragments sdRNA-D19b and -A24 emerged among the most differentially expressed and were selected for further experimentation. We found that the overexpression of either sdRNA significantly increased PC3 (a well-established model of castration-resistant prostate cancer (CRPC)) cell proliferation, and that sdRNA-D19b overexpression also markedly increased the rate of PC3 cell migration. In addition, both sdRNAs provided drug-specific resistances with sdRNA-D19b levels correlating with paclitaxel resistance and sdRNA-24A conferring dasatinib resistance. In silico and in vitro analyses revealed that two established PCa tumor suppressor genes, CD44 and CDK12, represent targets for sdRNA-D19b and sdRNA-A24, respectively. This outlines a biologically coherent mechanism by which sdRNAs downregulate tumor suppressors in AR-PCa to enhance proliferative and metastatic capabilities and to encourage chemotherapeutic resistance. Aggressive proliferation, rampant metastasis, and recalcitrance to chemotherapy are core characteristics of CRPC that synergize to produce a pathology that ranks second in cancer-related deaths for men. This study defines sdRNA-D19b and -A24 as contributors to AR-PCa, potentially providing novel biomarkers and therapeutic targets of use in PCa clinical intervention.

Indexed as

MicroRNAsProstatic Neoplasms, Castration-ResistantCell ProliferationHumansMalePC-3 CellsRNA, Small NucleolarMicroRNAsRNA, Small Nucleolarcancercastration-resistantCD44CDK12microRNAncRNAnoncoding RNAprostatesdRNAsnoRNA

Identifiers

PMID35455981
PMCPMC9032336
OpenAlexW4226070127

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.