Tributyrin, an oral butyrate analogue, induces apoptosis through the activation of caspase-3

The purpose of this study was to investigate the anti-proliferative and pro-apoptotic effects of the butyrate analogues, tributyrin (TB) and phenylbutyrate (PB), in a colon cancer model. We demonstrate that HT-29 colon cancer cells exposed to PB and TB result in growth inhibition associated with an...

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Bibliographic Details
Published in:Cancer letters 2001-09, Vol.171 (1), p.57-65
Main Authors: Clarke, Kevin O, Feinman, Rena, Harrison, Lawrence E
Format: Article
Language:English
Subjects:
Adenocarcinoma - enzymology
Adenocarcinoma - pathology
Antineoplastic agents
Antineoplastic Agents - pharmacology
Apoptosis
Apoptosis - drug effects
Biological and medical sciences
Butyrates - pharmacology
Caspase 3
Caspases - metabolism
CDC2-CDC28 Kinases
Cell cycle control
Cell Cycle Proteins
Chemotherapy
Colonic Neoplasms - enzymology
Colonic Neoplasms - pathology
Cyclin-Dependent Kinase 2
Cyclin-Dependent Kinases - metabolism
Differentiation
DNA-Binding Proteins - metabolism
E2F Transcription Factors
E2F4 Transcription Factor
Enzyme Activation - drug effects
Fatty acid
G1 Phase - drug effects
Medical sciences
Neoplasm Proteins - metabolism
Nuclear Proteins - metabolism
Pharmacology. Drug treatments
Phenotype
Phenylbutyrate
Phenylbutyrates - pharmacology
Phosphorylation - drug effects
Protein Processing, Post-Translational - drug effects
Protein-Serine-Threonine Kinases - metabolism
Retinoblastoma Protein - metabolism
Transcription Factors - metabolism
Tributyrin
Triglycerides - pharmacology
Tumor Cells, Cultured - drug effects
Tumor Cells, Cultured - enzymology
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Summary:The purpose of this study was to investigate the anti-proliferative and pro-apoptotic effects of the butyrate analogues, tributyrin (TB) and phenylbutyrate (PB), in a colon cancer model. We demonstrate that HT-29 colon cancer cells exposed to PB and TB result in growth inhibition associated with an induction of apoptosis mediated through the activation of caspase-3 activity. A block in the G1/S cell cycle traverse associated with a decrease in CDK2 (cyclin dependent kinase) protein levels and retinoblastoma protein hypophosphorylation was also noted after PB and TB exposure. Importantly, TB proved to be the most potent agent in its ability to induce these phenotypic changes, and potentially may represent a novel therapy for patients with advanced colorectal cancer.
ISSN:0304-3835
1872-7980
DOI:10.1016/S0304-3835(01)00574-2