Evidence map›Paper›PMID 24124611›Full record

ArticlePloS one2013

Delphinidin reduces cell proliferation and induces apoptosis of non-small-cell lung cancer cells by targeting EGFR/VEGFR2 signaling pathways.

Harish Chandra Pal, Samriti Sharma, Leah Ray Strickland, Jyoti Agarwal, Mohammad Athar, Craig A Elmets, Farrukh Afaq

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Pooled it
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  18. Delphinidin and Its Glycosides' War on Cancer: Preclinical Perspectives.International journal of molecular sciences · 2021
    Review
  19. The Hallmarks of Flavonoids in Cancer.Molecules (Basel, Switzerland) · 2021
    Review
  20. Article
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

7 authors at 1 institution in 1 country.

Harish Chandra PalDepartment of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Samriti Sharma
Leah Ray Strickland
Jyoti Agarwal
Mohammad Athar
Craig A Elmets
Farrukh Afaq
University of Alabama at Birmingham · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
Inhibiting Multiple Molecular Targets for Preventing Non-Melanoma Skin CancerR01CA138998 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ATHAR, MOHAMMAD · 2011 to 2015
$1.5M
Delphinidin: A Novel Agent For Treatment Of PsoriasisR21AT004966 · NCCIH · UNIVERSITY OF WISCONSIN-MADISON · PI AFAQ, FARRUKH · 2010 to 2011
$404k
NCCIH NIH HHS AT004966NCCIH NIH HHS R21 AT004966NCI NIH HHS CA13148-39NCI NIH HHS P30 CA013148NCI NIH HHS R01 CA138998
6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor 2 (VEGFR2) have emerged as two effective clinical targets for non-small-cell lung cancer (NSCLC). In the present study, we found that delphinidin, an anthocyanidin, present in pigmented fruits and vegetables, is a potent inhibitor of both EGFR and VEGFR2 in NSCLC cells that overexpress EGFR/VEGFR2. Using these cells, we next determined the effects of delphinidin on cell growth and apoptosis in vitro and on tumor growth and angiogenesis in vivo. Delphinidin (5-60 µM) treatment of NSCLC cells inhibited the activation of PI3K, and phosphorylation of AKT and MAPKs. Additionally, treatment of NSCLC cells with delphinidin resulted in inhibition of cell growth without having significant toxic effects on normal human bronchial epithelial cells. Specifically, treatment of NCI-H441 and SK-MES-1 cells with delphindin (5-60 µM) resulted in (i) cleavage of PARP protein, (ii) activation of caspase-3 and -9, (iii) downregulation of anti-apoptotic proteins (Bcl2, Bcl-xL and Mcl-1), (iv) upregulation of pro-apoptotic proteins (Bax and Bak), and (v) decreased expression of PCNA and cyclin D1. Furthermore, in athymic nude mice subcutaneously implanted with human NSCLC cells, delphinidin treatment caused a (i) significant inhibition of tumor growth, (ii) decrease in the expression of markers for cell proliferation (Ki67 and PCNA) and angiogenesis (CD31 and VEGF), and (iii) induction of apoptosis, when compared with control mice. Based on these observations, we suggest that delphinidin, alone or as an adjuvant to current therapies, could be used for the management of NSCLC, especially those that overexpress EGFR and VEGFR2.

Indexed as

AnimalsAnthocyaninsAntineoplastic Agents, PhytogenicApoptosisCarcinoma, Non-Small-Cell LungCaspasesCell Line, TumorCell ProliferationCyclin D1Disease Models, AnimalEpidermal Growth FactorErbB ReceptorsFemaleHumansLung NeoplasmsMiceAnthocyaninsAntineoplastic Agents, PhytogenicCaspasesCyclin D1delphinidinEpidermal Growth FactorErbB ReceptorsMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPoly(ADP-ribose) PolymerasesProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Vascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID24124611
PMCPMC3790876
OpenAlexW2062739811

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.