Evidence map›Paper›PMID 22348037›Full record

ArticlePloS one2012

EGCG enhances the therapeutic potential of gemcitabine and CP690550 by inhibiting STAT3 signaling pathway in human pancreatic cancer.

Su-Ni Tang, Junsheng Fu, Sharmila Shankar, Rakesh K Srivastava

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 94 citations in OpenAlex.

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  16. Anticarcinogenic potentials of tea catechins.Frontiers in nutrition · 2022
    Review
  17. Review
  18. Molecular Targets of Natural Compounds with Anti-Cancer Properties.International journal of molecular sciences · 2021
    Review
  19. 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

4 authors at 2 institutions in 1 country.

Su-Ni TangDepartment of Pharmacology, Toxicology and Therapeutics, and Medicine, The University of Kansas Cancer Center, The University of Kansas Medical Center, Kansas City, Kansas, United States of America.
Junsheng Fu
Sharmila Shankar
Rakesh K Srivastava
University of Kansas Medical Center · USThe University of Kansas Cancer Center · US

Funding

Chemoprevention of Pancreatic Cancer by EGCGR01CA125262 · NCI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI DHAR, ANIMESH · 2008 to 2012
$1.7M
Mechanisms of Chemoprevention by ResveratrolR01CA114469 · NCI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI SRIVASTAVA, RAKESH K. · 2005 to 2009
$726k
NCI NIH HHS R01 CA114469NCI NIH HHS R01CA114469NCI NIH HHS R01 CA125262NCI NIH HHS R01CA125262NCI NIH HHS R01CA125262-02S1
6 · The paper itself

Abstract

backgroundSignal Transducer and Activator of Transcription 3 (STAT3) is an oncogene, which promotes cell survival, proliferation, motility and progression in cancer cells. Targeting STAT3 signaling may lead to the development of novel therapeutic approaches for human cancers. Here, we examined the effects of epigallocathechin gallate (EGCG) on STAT3 signaling in pancreatic cancer cells, and assessed the therapeutic potential of EGCG with gemcitabine or JAK3 inhibitor CP690550 (Tasocitinib) for the treatment and/or prevention of pancreatic cancer. METHODOLOGY/PRINCIPAL

findingsCell viability and apoptosis were measured by XTT assay and TUNEL staining, respectively. Gene and protein expressions were measured by qRT-PCR and Western blot analysis, respectively. The results revealed that EGCG inhibited the expression of phospho and total JAK3 and STAT3, STAT3 transcription and activation, and the expression of STAT3-regulated genes, resulting in the inhibition of cell motility, migration and invasion, and the induction of caspase-3 and PARP cleavage. The inhibition of STAT3 enhanced the inhibitory effects of EGCG on cell motility and viability. Additionally, gemcitabine and CP690550 alone inhibited STAT3 target genes and synergized with EGCG to inhibit cell viability and induce apoptosis in pancreatic cancer cells. CONCLUSIONS/SIGNIFICANCE: Overall, these results suggest that EGCG suppresses the growth, invasion and migration of pancreatic cancer cells, and induces apoptosis by interfering with the STAT3 signaling pathway. Moreover, EGCG further enhanced the therapeutic potential of gemcitabine and CP690550 against pancreatic cancer.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsApoptosisCatechinCell Line, TumorCell MovementCell SurvivalDeoxycytidineDrug SynergismGemcitabineHumansPancreatic NeoplasmsPiperidinesPyrimidinesPyrrolesSignal TransductionSTAT3 Transcription FactorCatechinDeoxycytidineepigallocatechin gallateGemcitabinePiperidinesPyrimidinesPyrrolesSTAT3 Transcription Factortofacitinib

Identifiers

PMID22348037
PMCPMC3278426
OpenAlexW2057899102

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.