Evidence map›Paper›PMID 26485930›Full record

ArticleJournal of biomedical nanotechnology2015

Identification and Testing of Novel CARP-1 Functional Mimetic Compounds as Inhibitors of Non-Small Cell Lung and Triple Negative Breast Cancers.

Magesh Muthu, Jaganmohan Somagoni, Vino T Cheriyan, Sara Munie, Edi Levi, Abdelkader E Ashour, Alaa Eldeen B Yassin, Ahmed M Alafeefy, Paula Sochacki, Lisa A Polin and 4 more

Open access · greenAbstract read
In one paragraph

Article in Journal of biomedical nanotechnology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 21 citations in OpenAlex.

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  9. Role of nano-lipid formulation of CARP-1 mimetic, CFM-4.17 to improve systemic exposure and response in osimertinib resistant non-small cell lung cancer.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2021
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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

14 authors.

Magesh Muthu
Jaganmohan Somagoni
Vino T Cheriyan
Sara Munie
Edi Levi
Abdelkader E Ashour
Alaa Eldeen B Yassin
Ahmed M Alafeefy
Paula Sochacki
Lisa A Polin
Kaladhar B Reddy
Scott D Larsen
Mandip Singh
Arun K Rishi

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI Julie Lynn Boerner · 1985 to 2026
$68.4M
Targeted Nanocarrier Combination Based Therapy for Lung CancerP20MD006738 · NIMHD · FLORIDA AGRICULTURAL AND MECHANICAL UNIV · PI RAHMAN, SALEH MD. MAHMUDUR · 2012 to 2016
$5.6M
CARP-1: A Potential Therapeutic Agent for Breast CancerI01BX001164 · VA · JOHN D DINGELL VA MEDICAL CENTER · PI RISHI, ARUN KUMAR · 2012 to 2020
–
BLRD VA I01 BX001164NCI NIH HHS P30 CA022453NIGMS NIH HHS SC1 GM092779-01NIMHD NIH HHS 1P20 MD006738-03NIMHD NIH HHS P20 MD006738
6 · The paper itself

Abstract

The triple negative breast cancer (TNBCs) and non-small cell lung cancers (NSCLCs) often acquire mutations that contribute to failure of drugs in clinic and poor prognosis, thus presenting an urgent need to develop new and improved therapeutic modalities. Here we report that CARP-1 functional mimetic (CFMs) compounds 4 and 5, and 4.6, a structurally related analog of CFM-4, are potent inhibitors of TNBC and NSCLC cells in vitro. Cell growth suppression by CFM-4 and -4.6 involved interaction and elevated expression of CARP-1/CCAR1 and Death Effector Domain (DED) containing DNA binding (DEDD)2 proteins. Apoptosis by these compounds also involved activation of pro-apoptotic stress-activated kinases p38 and JNK1/2, cleavage of PARP and loss of mitotic cyclin B1. Both the CFMs inhibited abilities of NSCLC and TNBC cells to migrate, invade, and form colonies in suspension, while disrupting tubule formation by the human umbilical vein endothelial cells (HUVECs). Nano-lipid formulation of CFM-4 (CFM-4 NLF) enhanced its serum bioavailability when compared with the free CFM-4. Oral administration of CFM-4 NLF reduced weights and volume of the xenografted tumors derived from A549 NSCLC and MDA-MB-231 TNBC cells. Although no gross tissue or histological toxicities were noticed, the immuno-histochemical analysis revealed increased CARP-1 and DNA fragmentation in tumors of the CFM-4 NLF-treated animals. In conclusion, while stimulation of pro-apoptotic CARP-1 and DEDD2 expression and their binding underscore a novel mechanism of apoptosis transduction by CFM compounds, our proof-of-concept xenograft studies demonstrate therapeutic potential of CFM-4 for TNBC and NSCLC.

Indexed as

AnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsBiomimetic MaterialsCell Cycle ProteinsCell Line, TumorCell SurvivalDrug CompoundingFemaleMiceMice, NudeMice, SCIDNanoparticlesNeoplasms, ExperimentalTreatment OutcomeAntineoplastic AgentsApoptosis Regulatory ProteinsCCAR1 protein, mouseCell Cycle Proteins

Identifiers

PMID26485930
PMCPMC5090172
OpenAlexW2415978549

What OpenQuestion holds

Textmetadata
LicenceTDM
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.