Induction of Apoptosis in a Human Breast Cancer Cell Overexpressing ErbB-2 Receptor by α-Tocopheryloxybutyric Acid

Akihiko Akazawa; Kazuhiro Nishikawa; Kazuyuki Suzuki; Ryuji Asano; Itsumaru Kumadaki; Haruna Satoh; Kiyokazu Hagiwara; Sung Jae Shin; Tomohiro Yano

doi:10.1254/jjp.89.417

Short Communications

Induction of Apoptosis in a Human Breast Cancer Cell Overexpressing ErbB-2 Receptor by α-Tocopheryloxybutyric Acid

Akihiko Akazawa, Kazuhiro Nishikawa, Kazuyuki Suzuki, Ryuji Asano, Itsumaru Kumadaki, Haruna Satoh, Kiyokazu Hagiwara, Sung Jae Shin, Tomohiro Yano

Author information

Akihiko Akazawa
Department of Veterinary Pharmacology, College of Bioresource Sciences, Nihon University
Kazuhiro Nishikawa
Department of Veterinary Pharmacology, College of Bioresource Sciences, Nihon University
Kazuyuki Suzuki
Department of Veterinary Pharmacology, College of Bioresource Sciences, Nihon University
Ryuji Asano
Department of Veterinary Pharmacology, College of Bioresource Sciences, Nihon University
Itsumaru Kumadaki
Faculty of Pharmaceutical Sciences, Setsunan University
Haruna Satoh
Department of Food Science Research for Health, National Institute of Health and Nutrition
Kiyokazu Hagiwara
Department of Food Science Research for Health, National Institute of Health and Nutrition
Sung Jae Shin
Department of Food Science Research for Health, National Institute of Health and Nutrition
Tomohiro Yano
Department of Food Science Research for Health, National Institute of Health and Nutrition

Keywords: α-Tocopheryloxybutyric acid, Apoptosis, Breast cancer cell

JOURNAL FREE ACCESS

2002 Volume 89 Issue 4 Pages 417-421

DOI https://doi.org/10.1254/jjp.89.417

Details

Abstract

The overexpression of ErbB-2 receptor relates to malignant transformation of breast cancer. The present study was carried out to establish the usefulness of α-tocopheryloxybutyric acid (TE) as a chemotherapeutic agent for human breast cancer. TE caused induction of apoptosis in MDA-MB-453 cells overexpressing the ErbB-2 receptor. TE reduced levels of activated ErbB-2 receptor and Akt. In contrast, TE induced the activation of p38, and SB203580, a specific inhibitor for p38, attenuated the TE-induced apoptosis. These data indicate that simultaneous occurrences of Akt inhibition and p38 activation by TE result in the cell death.

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