Evidence map›Paper›PMID 41954995›Full record

ArticleOncotarget2026

CREB5 regulates stem cell-like transcriptional programs to enhance tumor progression in prostate cancer.

Allison Makovec, John T Phoenix, Hannah E Bergom, Ella Boytim, Ava P Gustafson, Aiden Deacon, Sydney Tape, Atef Ali, Megan Ludwig, Samuel P Pitzen and 14 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

24 authors.

Allison MakovecDepartment of Medicine, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
John T PhoenixDepartment of Cancer Biology, Loyola University Chicago, Chicago, IL 60153, USA.
Hannah E BergomDepartment of Medicine, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Ella BoytimDepartment of Medicine, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Ava P GustafsonDepartment of Medicine, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Aiden DeaconCancer Biology Graduate Program, University of Colorado Anschutz, Aurora, CO 80045, USA.
Sydney TapeMedical College of Wisconsin, Green Bay, WI 54115, USA.
Atef AliBioinformatic Interdepartmental Program, University of California, Los Angeles, CA 90095, USA.
Megan LudwigMasonic Cancer Center, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Samuel P PitzenMasonic Cancer Center, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
David MolineDepartment of Medicine, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Camden RichterRush University Medical College, Chicago, IL 60612, USA.
Hudson LongieDepartment of Medicine, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Mei-Chi SuDepartment of Experimental and Clinical Pharmacology, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Sampreeti JenaDepartment of Experimental and Clinical Pharmacology, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Pornlada LikasitwatanakulDepartment of Medicine, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Justin M DrakeMasonic Cancer Center, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
R Stephanie HuangMasonic Cancer Center, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
William C HahnBroad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Jonathan P RennhackDepartment of Cancer Biology, Loyola University Chicago, Chicago, IL 60153, USA.
Scott M DehmMasonic Cancer Center, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Steven KregelDepartment of Cancer Biology, Loyola University Chicago, Chicago, IL 60153, USA.
Emmanuel S AntonarakisDepartment of Medicine, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.
Justin HwangDepartment of Medicine, University of Minnesota - Twin Cities, Minneapolis, MN 55455, USA.

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Timothy C. Hallstrom · 1998 to 2026
$100.4M
Genetic mechanisms underlying sexual dimorphism in cancer and response to therapyR01CA229618 · NCI · UNIVERSITY OF COLORADO DENVER · PI HUANG, RONG STEPHANIE, STRANGER, BARBARA E · 2019 to 2024
$2.9M
Drug repurposing in breast cancerR01CA204856 · NCI · UNIVERSITY OF MINNESOTA · PI HUANG, RONG STEPHANIE · 2018 to 2022
$2.2M
DOD W81XWH-22-2-0025NCI NIH HHS P30 CA077598NCI NIH HHS R01 CA204856NCI NIH HHS R01 CA229618
6 · The paper itself

Abstract

Copyright: © 2026 Makovec et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Prostate gland cells can be transcriptionally and morphologically characterized as basal and luminal. About 30–40% of advanced prostate cancers (PC) harbor basal-like transcription programs. In castration-resistant PC (CRPC), studies indicate that basal and stem cell-like (SCL) tumors are major resistance mechanisms to androgen receptor (AR)-targeted therapies. SCL tumors have reduced AR activity and increased stem-cell activity that promotes tumor formation, which contributes to poor clinical outcomes. We determined that CREB5 is a key regulator of basal and SCL transcriptional programs and tumor-forming phenotypes in PC. Through in silico modeling of PC transcriptomes and several pre-defined PC signaling programs, CREB5 expression was best associated with basal-like gene signatures and SCL-associated genes in primary PC and CRPCs (n = 493 and 208). This included associations with FOSL1 and other AP-1 transcription factors. We further found that CREB5 interacted with AP-1 proteins and bound to the regulatory elements of AP-1 genes, suggesting a mechanistic role in regulating the activity of AP-1 genes. In AR-positive cells, CREB5 overexpression promoted cell colony growth with tumorigenic properties and increased tumor size in vivo. These findings implicate CREB5 as a driver of the transcriptional programs underlying AR-independent basal and SCL CRPC subtypes, and this activity is detectable in primary PC.

Indexed as

Cyclic AMP Response Element-Binding ProteinGene Expression Regulation, NeoplasticNeoplastic Stem CellsProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantAnimalsCell Line, TumorDisease ProgressionHumansMaleMiceReceptors, AndrogenSignal TransductionTranscription Factor AP-1Transcription, GeneticCyclic AMP Response Element-Binding ProteinReceptors, AndrogenTranscription Factor AP-1AP-1 transcription factorsbasal-likeCREB5prostate cancerstem cell-like

Identifiers

PMID41954995
PMCPMC13064935

What OpenQuestion holds

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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.