Evidence map›Paper›PMID 41087459›Full record

ArticleScientific reports2025

A novel D-peptide modulates DCLK1 gelsolin interactions, reducing PDAC tumor growth.

Landon L Moore, Dongfeng Qu, Parthasarathy Chandrekesan, Kamille Pitts, Randal May, Byron E Anderson, Milton L Brown, Courtney W Houchen

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

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No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Landon L MooreDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Dongfeng QuDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Parthasarathy ChandrekesanDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Kamille PittsDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Randal MayDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Byron E Anderson, Chicago, IL, USA.
Milton L BrownDepartment of Internal Medicine, Macon & Joan Brock Virginia Health Sciences at Old Dominion University, Norfolk, VA, 23507, USA.
Courtney W HouchenDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA. courtney-houchen@ouhsc.edu.

Funding

Tissue Pathology Shared ResourceP30CA225520 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Michael S. Businelle · 2018 to 2026
$27.1M
National Cancer Institute (NCI) Cancer Center Support Grant P30CA225520NCI NIH HHS P30 CA225520Oklahoma Tobacco Settlement Endowment Trust R23-02Presbyterian Health Foundation Bridge
6 · The paper itself

Abstract

What drives inflammation-associated tumorigenesis and progression in pancreatic ductal adenocarcinoma (PDAC)? Doublecortin-like kinase 1 (DCLK1) is a central driver of inflammation-associated tumorigenesis, with elevated expression linked to worse clinical outcomes. Two isoforms of DCLK1 possess a unique extracellular domain (ECD). DCLK1 isoform 2 contains two microtubule-binding domains, while isoform 4, lacks the microtubule-binding domains but, plays a pivotal role in tumor progression. We identified novel D-peptides that selectively target this ECD, significantly suppressing PDAC cell proliferation in vitro and tumor growth in xenograft models without inducing cell death. In silico modeling and binding assays revealed DCLK1 isoform 4 interacts with pro-tumorigenic proteins like plasma gelsolin (pGSN), with D-peptides modulating these interactions. These findings underscore DCLK1's non-kinase functions as a therapeutic target and highlight novel avenues for developing precision treatments aimed at halting cancer progression and improving patient outcomes.

Indexed as

Carcinoma, Pancreatic DuctalGelsolinIntracellular Signaling Peptides and ProteinsPancreatic NeoplasmsPeptidesProtein Serine-Threonine KinasesAnimalsCell Line, TumorCell ProliferationDoublecortin-Like KinasesHumansMiceProtein BindingXenograft Model Antitumor AssaysDCLK1 protein, humanDoublecortin-Like KinasesGelsolinIntracellular Signaling Peptides and ProteinsPeptidesProtein Serine-Threonine KinasesDCLK1D-peptidesGelsolinPancreatic ductal adenocarcinoma (PDAC)

Identifiers

PMID41087459
PMCPMC12521541

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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.