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Epicatechin gallate-induced expression of NAG-1 is associated with growth inhibition and apoptosis in colon cancer cells.

Epicatechin gallate-induced expression of NAG-1 is associated with growth inhibition and apoptosis in colon cancer cells. Research Abstract Details 

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  • Epicatechin gallate-induced expression of NAG-1 is associated with growth inhibition and apoptosis in colon cancer cells. Abstract Text:

    seung joon baekSeung Joon Baek,jong-sik kimJong-Sik Kim,felix r jacksonFelix R Jackson,thomas e elingThomas E Eling,michael f mcenteeMichael F McEntee,seong-ho leeSeong-Ho Lee,

    There is persuasive epidemiological and experimental evidence that dietary polyphenolic plant-derived compounds have anticancer activity. Many laboratories, including ours, have reported such an effect in cancers of the gastrointestinal tract, lung, skin, prostate and breast. The catechins are a group of polyphenols found in green tea, which is one of the most commonly consumed beverages in the world. While the preponderance of the data strongly indicates significant antitumorigenic benefits from the green tea catechins, the potential molecular mechanisms involved remain obscure. We found that green tea components induce apoptosis via a TGF-beta superfamily protein, NAG-1 (Non-steroidal anti-inflammatory drug Activated Gene). In this report, we show that ECG is the strongest NAG-1 inducer among the tested catechins and that treatment of HCT-116 cells results in an increasing G(1) sub-population, and cleavage of poly (ADP-ribose) polymerase (PARP), consistent with apoptosis. In contrast, other catechins do not significantly induce NAG-1 expression, PARP cleavage or morphological changes at up to a 50-microM concentration. Furthermore, we provide evidence that ECG induces the ATF3 transcription factor, followed by NAG-1 induction at the transcriptional level in a p53-independent manner. The data generated by this study will help elucidate mechanisms of action for components in green tea and this information may lead to the design of more effective anticancer agents and informed clinical trials.

    Epicatechin gallate-induced expression of NAG-1 is associated with growth inhibition and apoptosis in colon cancer cells. Publishing Authors By Initials

    sj baekSJ Baek,js kimJS Kim,fr jacksonFR Jackson,te elingTE Eling,mf mcenteeMF McEntee,sh leeSH Lee,

    For similar proteins: dna-binding proteins: tumor suppressor protein p53 research abstracts see: proteins: dna-binding proteins: tumor suppressor protein p53 research

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    Epicatechin gallate-induced expression of NAG-1 is associated with growth inhibition and apoptosis in colon cancer cells. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: Carcinogenesis

    VOLUME: 25

    Page Numbers: 2425-32

    Journal Abbreviation: Carcinogenesis

    ISSN: 0143-3334

    DAY: 12

    MONTH: 08

    YEAR: 2004

    Epicatechin gallate-induced expression of NAG-1 is associated with growth inhibition and apoptosis in colon cancer cells. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8008055

    Epicatechin gallate-induced expression of NAG-1 is associated with growth inhibition and apoptosis in colon cancer cells. Keywords Mesh Terms:

    KEYWORDS: Tumor Suppressor Protein p53

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Epicatechin gallate-induced expression of NAG-1 is associated with growth inhibition and apoptosis in colon cancer cells. Information

    Substance Name: Poly(ADP-ribose) Polymerases

    Registry Number: EC 2.4.2.30

    Grant and Affiliation Information for Epicatechin gallate-induced expression of NAG-1 is associated with growth inhibition and apoptosis in colon cancer cells.

    AFFILIATION: Laboratory of Environmental Carcinogenesis, Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, 2407 River Drive, Knoxville, TN 37996, USA. sbaek2@utk.edu

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NIEHS

    GRANT: K22ES011657

    ACRONYM: ES

    MEDLINETA: Carcinogenesis

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    ACCESSION NUMBER:

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