Evidence map›Paper›PMID 22322442›Full record

ArticleInternational journal of cancer2012

Plumbagin, a plant derived natural agent inhibits the growth of pancreatic cancer cells in in vitro and in vivo via targeting EGFR, Stat3 and NF-κB signaling pathways.

Bilal Bin Hafeez, Mohammad Sarwar Jamal, Joseph W Fischer, Ala Mustafa, Ajit Kumar Verma

Open access · greenAbstract read
In one paragraph

Article in International journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Phytochemicals fromMicroorganisms · 2025
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  18. Inhibitory Effects of Plumbagin on Retinal Pigment Epithelial Cell Epithelial-Mesenchymal Transition In Vitro and In Vivo.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
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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

5 authors at 2 institutions in 1 country.

Bilal Bin HafeezDepartment of Human Oncology, Wisconsin Institute of Medical Research, Paul Carbone Comprehensive Cancer Center, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53792, USA. hafeez@humonc.wisc.edu
Mohammad Sarwar Jamal
Joseph W Fischer
Ala Mustafa
Ajit Kumar Verma
University of Wisconsin Carbone Cancer Center · USUniversity of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Christian Capitini · 1985 to 2026
$142.6M
Role of PKC in Tumor PromotionR01CA035368 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI VERMA, AJIT K · 1985 to 2011
$3.6M
NCI NIH HHS CA35368NCI NIH HHS P30 CA014520NCI NIH HHS R01 CA035368
6 · The paper itself

Abstract

Pancreatic cancer (PC) is the most aggressive malignant disease, ranks as the fourth most leading cause of cancer-related death among men and women in the United States. We present here that plumbagin (PL), a quinoid constituent isolated from the roots of the medicinal plant Plumbago zeylanica L, inhibits the growth of PC cells both in vitro and in vivo model systems. PL treatment induces apoptosis and inhibits cell viability of PC cells (PANC1, BxPC3 and ASPC1). In addition, i.p. administration of PL (2 mg/kg body weight, 5 days a week) in severe combined immunodeficiency (SCID) mice beginning 3 days after ectopic implantation of PANC1 cells resulted in a significant (P < 0.01) inhibition of both tumor weight and volume. PL treatment inhibited (1) constitutive expression of epidermal growth factor receptor (EGFR), pStat3Tyr705 and pStat3Ser727, (2) DNA binding of Stat3 and (3) physical interaction of EGFR with Stat3, in both cultured PANC1 cells and their xenograft tumors. PL treatment also inhibited phosphorylation and DNA-binding activity of NF-κB in both cultured PC cells (PANC1 and ASPC1) and in PANC1 cells xenograft tumors. Downstream target genes (cyclin D1, MMP9 and Survivin) of Stat3 and NF-κB were similarly inhibited. These results suggest that PL may be used as a novel therapeutic agent against human PC. Published 2012 Wiley-Liss, Inc. This article is a US Government work, and, as such, is in the public domain in the United States of America.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicApoptosisCell Line, TumorCell ProliferationCyclin D1ErbB ReceptorsHumansInhibitor of Apoptosis ProteinsMaleMatrix Metalloproteinase InhibitorsMiceMice, SCIDNaphthoquinonesNF-kappa BPancreatic NeoplasmsAntineoplastic Agents, PhytogenicBIRC5 protein, humanCyclin D1ErbB ReceptorsInhibitor of Apoptosis ProteinsMatrix Metalloproteinase InhibitorsNaphthoquinonesNF-kappa BPlant ExtractsplumbaginSTAT3 protein, humanSTAT3 Transcription FactorSurvivin

Identifiers

PMID22322442
PMCPMC3522120
OpenAlexW2063382047

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.