Evidence map›Paper›PMID 19369860›Full record

ArticleAnti-cancer drugs2009

The marine alkaloid naamidine A promotes caspase-dependent apoptosis in tumor cells.

Daniel V LaBarbera, Katarzyna Modzelewska, Amanda I Glazar, Phillip D Gray, Manjinder Kaur, Tong Liu, Douglas Grossman, Mary Kay Harper, Scott K Kuwada, Nadeem Moghal and 1 more

Open access · greenAbstract read
In one paragraph

Article in Anti-cancer drugs, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.9field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 45 citations in OpenAlex.

  1. TargetingFrontiers in bioinformatics · 2025
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  9. Total synthesis and cytotoxicity of Leucetta alkaloids.Bioorganic & medicinal chemistry · 2017
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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

11 authors at 5 institutions in 3 countries.

Daniel V LaBarberaDepartment of Medicinal Chemistry University of Utah, Salt Lake City, UT 84112, USA.
Katarzyna Modzelewska
Amanda I Glazar
Phillip D Gray
Manjinder Kaur
Tong Liu
Douglas Grossman
Mary Kay Harper
Scott K Kuwada
Nadeem Moghal
Chris M Ireland
University of Utah · USInstitute of Medicinal Plant Development · CNUniversity of Colorado Anschutz Medical Campus · USHuntsman Cancer Institute · USUniversity Health Network · CA

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
MULTIDISCIPLINARY CANCER RESEARCH TRAINING PROGRAMT32CA093247 · NCI · UNIVERSITY OF UTAH · PI AYER, DONALD E · 2002 to 2011
$5.2M
ANTINEOPLASTIC AGENTS FROM MARINE ORGANISMSR01CA036622 · NCI · UNIVERSITY OF UTAH · PI IRELAND, CHRIS M. · 1985 to 2010
$3.0M
Regulation of apoptosis in melanocytic cellsR01AR050102 · NIAMS · UNIVERSITY OF UTAH · PI GROSSMAN, DOUGLAS · 2004 to 2008
$1.3M
NCI NIH HHS CA36622NCI NIH HHS P30 CA042014NCI NIH HHS R01 CA036622NCI NIH HHS T32 CA093247NIAMS NIH HHS AR050102NIAMS NIH HHS R01 AR050102
6 · The paper itself

Abstract

Apoptosis is important for normal development and removal of damaged cells. Evasion of apoptosis by cancer cells is one of the key characteristics of many tumor types. Thus, discovering agents that promote apoptosis in tumor cells could have great therapeutic value. Marine natural products have demonstrated great potential as anticancer agents, and the proapoptotic activity of some of these products is emerging as a potentially useful property for cancer treatments. Using a tumor xenograft assay in rodents, we previously found that the marine alkaloid naamidine A is a potent antitumor agent. In this study, we further characterize the mechanism of action of naamidine A. In cultured tumor cells, we find that naamidine A induces cell death, which is accompanied with annexin V staining, disruption of the mitochondrial membrane potential, and cleavage and activation of caspases 3, 8, and 9, all of which are hallmarks of apoptosis. Furthermore, naamidine A-induced cell death is caspase dependent. We also find that under conditions where naamidine A inhibits tumor xenograft growth, it induces activation of caspase 3, suggesting that apoptosis is part of its antitumorigenic activity in vivo. Apoptosis is not dependent on extracellular signal-regulated kinase 1/2, previously characterized molecular targets of naamidine A, nor does it require functional p53. Our studies support the continued study of naamidine A and its target(s) for the potential development of better clinical treatments for cancer.

Indexed as

AlkaloidsAnimalsAntineoplastic AgentsApoptosisCaspasesCell Culture TechniquesCell CycleCell Line, TumorDose-Response Relationship, DrugDrug Screening Assays, AntitumorHumansImidazolesMiceMice, NudeNeoplasms, ExperimentalNeoplasm TransplantationAlkaloidsAntineoplastic AgentsCaspasesImidazolesnaamidine A

Identifiers

PMID19369860
PMCPMC7992254
OpenAlexW2073605475

What OpenQuestion holds

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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.