Tributyrin, an oral butyrate analogue, induces apoptosis through the activation of caspase-3
Authors: Clarke K.O.; Feinman R.; Harrison L.E.1
Source: Cancer Letters, Volume 171, Number 1, 28 August 2001, pp. 57-65(9)
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.
Keywords: Fatty acid; Phenylbutyrate; Tributyrin; Apoptosis; Cell cycle control; Differentiation
Document Type: Short communication
Affiliations: 1: Department of Surgery, UMDNJ - New Jersey Medical School, 185 South Orange Avenue, MSB G588, 07103, Newark, NJ, USA