Evidence map›Paper›PMID 42121927›Full record

ArticleCells2026

Dpep, a Cell-Penetrating Peptide Targeting ATF5, CEBPB and CEBPD, Synergistically Combines with ABT-263 and Decitabine to Inhibit Cancer Cell Growth and Overcome Dpep Resistance.

Qing Zhou, Trang Thi Thu Nguyen, James M Angelastro, Markus D Siegelin, Lloyd A Greene

Abstract read
In one paragraph

Article in Cells, 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

5 authors.

Qing ZhouDepartment of Pathology and Cell Biology, Vagelos College of Physicians & Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA.
Trang Thi Thu NguyenDepartment of Pathology and Cell Biology, Vagelos College of Physicians & Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA.ORCID 0000-0001-8747-9082
James M AngelastroDepartment of Molecular Biosciences, School of Veterinary Medicine, University of California Davis, Davis, CA 95616, USA.ORCID 0000-0001-5612-1221
Markus D SiegelinDepartment of Pathology and Cell Biology, Vagelos College of Physicians & Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA.
Lloyd A GreeneDepartment of Pathology and Cell Biology, Vagelos College of Physicians & Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA.ORCID 0000-0002-3225-5521

Funding

Neuron death in Parkinson's disease: The role of Trib3R01NS072050 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GREENE, LLOYD A · 2012 to 2022
$3.7M
HDAC Inhibitors Reverse the Warburg Effect and Elicit Metabolic Vulnerabilities in Model Systems of GlioblastomaR01NS113793 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SIEGELIN, MARKUS D · 2021 to 2025
$2.0M
Using Cell-Penetrant Peptides to Target ATF5 in Mouse Glioma ModelsR01NS083795 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ANGELASTRO, JAMES M · 2014 to 2018
$1.6M
Targeting OGDH for Glioblastoma TherapyR21NS137660 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SIEGELIN, MARKUS D · 2024 to 2025
$452k
NINDS NIH HHS R01NS072050NINDS NIH HHS R01 NS083795NINDS NIH HHS R01NS083795NINDS NIH HHS R01NS113793NINDS NIH HHS R21NS137660
6 · The paper itself

Abstract

Dpep is a cell-penetrating peptide that targets transcription factors ATF5, CEBPB and CEBPD to selectively suppress growth and survival of diverse tumor cell types in vitro and in vivo. Due to these actions and its apparent safety, the peptide has potential as a cancer therapeutic. How Dpep might be combined with other anti-cancer agents to achieve synergistic efficacy and to overcome possible peptide resistance has not been assessed in depth. Based on prior work indicating that Dpep promotes apoptotic cancer cell death and up-regulates multiple pro-apoptotic and tumor suppressor genes, we studied combinations of Dpep with ABT-263, a pro-apoptotic BCL2 family inhibitor, and decitabine, a hypomethylating drug. Combining Dpep with each agent alone or together synergistically suppressed the growth of a range of solid and liquid tumor cell types. Moreover, the combinations synergistically inhibited the growth of cells lines that were selected either in vivo or in vitro for Dpep resistance. Finally, we tested the combination of Dpep with ABT-263 in a mouse melanoma xenograft model. The combination more effectively inhibited tumor growth than either agent alone and, in contrast to vehicle or ABT-263, produced a 40% durable survival rate. Taken together, these observations highlight potential drug partners for the therapeutic development of Dpep.

Indexed as

Activating Transcription FactorsAniline CompoundsCell-Penetrating PeptidesDecitabineDrug Resistance, NeoplasmSulfonamidesAnimalsApoptosisCell Line, TumorCell ProliferationDrug SynergismFemaleHumansMiceMice, NudeXenograft Model Antitumor AssaysActivating Transcription FactorsAniline CompoundsCell-Penetrating PeptidesDecitabinenavitoclaxSulfonamidesABT-263anti-cancerapoptosisBpepcancercell-penetrating peptidecombination therapydecitabineDpepovercoming resistance

Identifiers

PMID42121927
PMCPMC13162579

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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.