1. Academic Validation
  2. Induction of apoptosis and caspase-3 activation by chemopreventive [6]-paradol and structurally related compounds in KB cells

Induction of apoptosis and caspase-3 activation by chemopreventive [6]-paradol and structurally related compounds in KB cells

  • Cancer Lett. 2002 Mar 8;177(1):41-7. doi: 10.1016/s0304-3835(01)00781-9.
Young Sam Keum 1 Jin Kim Keun Hyung Lee Kwang Kyun Park Young Joon Surh Jong Min Lee Sang Sup Lee Jung Hoon Yoon So Yeon Joo In Ho Cha Jong In Yook
Affiliations

Affiliation

  • 1 Oral Cancer Research Institute, Department of Oral Pathology and Oral Biology, College of Dentistry, Yonsei University, Seoul 120-752, South Korea.
Abstract

[6]-paradol, a pungent phenolic substance found in ginger and other Zingiberaceae plants, has been demonstrated to be an effective inhibitor of tumor promotion in mouse skin carcinogenesis. In the present study, we found that [6]-paradol and other structurally related derivatives, [10]-paradol, [3]-dehydroparadol, [6]-dehydroparadol, and [10]-dehydroparadol, with the exception of [3]-paradol induce Apoptosis in an oral squamous carcinoma cell line, KB, in a dose-dependent manner. [10]-paradol and [10]-dehydroparadol exhibited a similar extent of cytotoxicity to that of [6]-paradol. [6]-Dehydroparadol and [3]-dehydroparadol appeared to be more potent, with an IC50 less than 40 microM. Treatment of KB cells with an apoptosis-inducing concentration of [6]-dehydroparadol caused induction of proteolytic cleavage of pro-caspase-3. These results suggest that [6]-paradol and structurally related derivatives induce Apoptosis through a caspase-3-dependent mechanism.

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