Evidence map›Paper›PMID 25866249›Full record

ArticleMolecular cell2015

Caspase-3 promotes genetic instability and carcinogenesis.

Xinjian Liu, Yujun He, Fang Li, Qian Huang, Takamitsu A Kato, Russell P Hall, Chuan-Yuan Li

Open access · greenAbstract read
In one paragraph

Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

162 citing papers in PubMed, 255 citations in OpenAlex.

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  12. Wound-Healing Efficacy ofPharmaceuticals (Basel, Switzerland) · 2025
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102 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Xinjian LiuDepartment of Dermatology, Duke University Medical Center, Durham, NC 27710, USA.
Yujun HeDepartment of General Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China.
Fang LiDepartment of Dermatology, Duke University Medical Center, Durham, NC 27710, USA.
Qian HuangCancer Center, First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.
Takamitsu A KatoDepartment of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO 80523, USA.
Russell P HallDepartment of Dermatology, Duke University Medical Center, Durham, NC 27710, USA.
Chuan-Yuan LiDepartment of Dermatology, Duke University Medical Center, Durham, NC 27710, USA; Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA. Electronic address: chuan.li@duke.edu.
Duke University Hospital · USColorado State University · USDaping Hospital · CNShanghai First People's Hospital · CN

Funding

Pro-oncogenic roles of apoptotic caspasesR01ES024015 · NIEHS · DUKE UNIVERSITY · PI LI, CHUAN-YUAN · 2014 to 2018
$1.8M
The "Phoenix Rising" pathway of tumor repopulation during radiotherapyR01CA155270 · NCI · DUKE UNIVERSITY · PI LI, CHUAN-YUAN · 2011 to 2015
$1.6M
Molecular mechanisms of tumor response to cytotoxic chemotherapyR01CA136748 · NCI · UNIVERSITY OF COLORADO DENVER · PI LI, CHUAN-YUAN · 2009 to 2014
$1.5M
HIF genes in head and neck cancer radiotherapyR01CA131408 · NCI · UNIVERSITY OF COLORADO DENVER · PI LI, CHUAN-YUAN · 2009 to 2014
$1.5M
Tissue Procurement and Analysis CoreP30AR066527 · NIAMS · DUKE UNIVERSITY · PI HALL, RUSSELL P. · 2014 to 2015
$1.3M
NCI NIH HHS CA131408NCI NIH HHS CA136748NCI NIH HHS CA155270NCI NIH HHS R01 CA131408NCI NIH HHS R01 CA136748NCI NIH HHS R01 CA155270NIAMS NIH HHS AR066527NIAMS NIH HHS P30 AR066527NIEHS NIH HHS ES024015NIEHS NIH HHS R01 ES024015
6 · The paper itself

Abstract

Apoptosis is typically considered an anti-oncogenic process since caspase activation can promote the elimination of genetically unstable or damaged cells. We report that a central effector of apoptosis, caspase-3, facilitates rather than suppresses chemical- and radiation-induced genetic instability and carcinogenesis. We found that a significant fraction of mammalian cells treated with ionizing radiation can survive despite caspase-3 activation. Moreover, this sublethal activation of caspase-3 promoted persistent DNA damage and oncogenic transformation. In addition, chemically induced skin carcinogenesis was significantly reduced in mice genetically deficient in caspase-3. Furthermore, attenuation of EndoG activity significantly reduced radiation-induced DNA damage and oncogenic transformation, identifying EndoG as a downstream effector of caspase-3 in this pathway. Our findings suggest that rather than acting as a broad inhibitor of carcinogenesis, caspase-3 activation may contribute to genome instability and play a pivotal role in tumor formation following damage.

Indexed as

Genomic Instability9,10-Dimethyl-1,2-benzanthraceneAnimalsBone Marrow CellsBreastCaspase 3Cells, CulturedEndodeoxyribonucleasesEpithelial CellsFemaleGenomeHumansMiceNeoplasms, ExperimentalSkin NeoplasmsTetradecanoylphorbol Acetate9,10-Dimethyl-1,2-benzanthraceneCASP3 protein, humanCasp3 protein, mouseCaspase 3Endodeoxyribonucleasesendonuclease GTetradecanoylphorbol Acetate

Identifiers

PMID25866249
PMCPMC4408780
OpenAlexW2002049273

What OpenQuestion holds

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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.