Nonsteroidal anti-inflammatory drugs induce colorectal cancer cell apoptosis by suppressing 14-3-3epsilon.

Nonsteroidal anti-inflammatory drugs induce colorectal cancer cell apoptosis by suppressing 14-3-3epsilon. Research Abstract Details 

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Nonsteroidal anti-inflammatory drugs induce colorectal cancer cell apoptosis by suppressing 14-3-3epsilon. Abstract Text:

Jun-Yang Liou,Dipak Ghelani,Sam Yeh,Kenneth K Wu,

To determine the role of 14-3-3 in colorectal cancer apoptosis induced by nonsteroidal anti-inflammatory drugs (NSAIDs), we evaluated the effects of sulindac on 14-3-3epsilon protein expression in colorectal cancer cells. Sulindac sulfide inhibited 14-3-3epsilon proteins in HT-29 and DLD-1 cells in a time- and concentration-dependent manner. Sulindac sulfone at 600 mumol/L inhibited 14-3-3epsilon protein expression in HT-29. Indomethacin and SC-236, a selective cyclooxygenase-2 (COX-2) inhibitor, exerted a similar effect as sulindac. Sulindac suppressed 14-3-3epsilon promoter activity. As 14-3-3epsilon promoter activation is mediated by peroxisome proliferator-activated receptor delta (PPARdelta), we determined the correlation between 14-3-3epsilon inhibition and PPARdelta suppression by NSAIDs. Sulindac sulfide inhibited PPARdelta protein expression and PPARdelta transcriptional activity. Overexpression of PPARdelta by adenoviral transfer rescued 14-3-3epsilon proteins from elimination by sulindac or indomethacin. NSAID-induced 14-3-3epsilon suppression was associated with reduced cytosolic Bad with elevation of mitochondrial Bad and increase in apoptosis which was rescued by Ad-PPARdelta transduction. Stable expression of 14-3-3epsilon in HT-29 significantly protected cells from apoptosis. Our findings shed light on a novel mechanism by which NSAIDs induce colorectal cancer apoptosis via the PPARdelta/14-3-3epsilon transcriptional pathway. These results suggest that 14-3-3epsilon is a target for the prevention and therapy of colorectal cancer.

Nonsteroidal anti-inflammatory drugs induce colorectal cancer cell apoptosis by suppressing 14-3-3epsilon. Publishing Authors By Initials

JY Liou,D Ghelani,S Yeh,KK Wu,

For similar peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-associated death protein research abstracts see: peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-associated death protein research

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MEDLINE DATE:

Nonsteroidal anti-inflammatory drugs induce colorectal cancer cell apoptosis by suppressing 14-3-3epsilon. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Cancer research

VOLUME: 67

Page Numbers: 3185-91

Journal Abbreviation:

ISSN: 0008-5472

DAY: 1

MONTH: Apr

YEAR: 2007

Nonsteroidal anti-inflammatory drugs induce colorectal cancer cell apoptosis by suppressing 14-3-3epsilon. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2984705

Nonsteroidal anti-inflammatory drugs induce colorectal cancer cell apoptosis by suppressing 14-3-3epsilon. Keywords Mesh Terms:

KEYWORDS: bcl-Associated Death Protein

MESH TERMS: metabolism

Chemical & Substance for Abstract: Nonsteroidal anti-inflammatory drugs induce colorectal cancer cell apoptosis by suppressing 14-3-3epsilon. Information

Substance Name: sulindac sulfone

Registry Number: 59864-04-9

Grant and Affiliation Information for Nonsteroidal anti-inflammatory drugs induce colorectal cancer cell apoptosis by suppressing 14-3-3epsilon.

AFFILIATION: University of Texas Health Science Center, M. D. Anderson Cancer Center, Houston, Texas, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL-50675

ACRONYM: HL

MEDLINETA: Cancer Res

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