alpha-Tocopheryloxybutyric acid enhances necrotic cell death in breast cancer cells treated with chemotherapy agent.

Abstract	The overexpression of HER-2 receptor contributes to malignant transformation of breast cancer cells. We have reported that alpha-tocopheryloxybutyric acid (TE), non-antioxidative vitamin E ether derivative inhibits the activation of HER-2 receptor. The present study was undertaken to estimate if TE could act as a useful anti-cancer agent against a breast cancer cell overexpressing HER-2 receptor (MDA-MB-453 cell line) in combination with a conventional chemotherapy agent, adriamycin (ADR). TE enhanced cytotoxic effect of ADR against the human breast cancer cell at low doses less than IC(50). The enhancing effect was mainly dependent on the elevation of necrotic-like cell death but not apoptotic cell death. In conjugation with this event, the inactivation of HER-2 receptor in the breast cancer cell was caused by the combination of TE with ADR. These results suggest that TE enhances necrotic-like cell death in the breast cancer cells and that the cell death relates to the inactivation of HER-2 receptor in the breast cancer cells.
Authors	Kazuhiro Nishikawa, Haruna Satoh, Ayako Hirai, Kazuyuki Suzuzki, Ryuji Asano, Itsumaro Kumadaki, Kiyokazu Hagiwara, Tomohiro Yano
Journal	Cancer letters (Cancer Lett) Vol. 201 Issue 1 Pg. 51-6 (Nov 10 2003) ISSN: 0304-3835 [Print] Ireland
PMID	14580686 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Antibiotics, Antineoplastic Proto-Oncogene Proteins tocopheryloxybutyric acid Vitamin E Doxorubicin Receptor, ErbB-3 Protein Serine-Threonine Kinases Proto-Oncogene Proteins c-akt
Topics	Antibiotics, Antineoplastic (pharmacology) Breast Neoplasms (drug therapy, pathology) Cell Line, Tumor Dose-Response Relationship, Drug Doxorubicin (pharmacology) Humans Immunoblotting Necrosis Protein Serine-Threonine Kinases Proto-Oncogene Proteins (drug effects, metabolism) Proto-Oncogene Proteins c-akt Receptor, ErbB-3 (drug effects, metabolism) Vitamin E (analogs & derivatives, pharmacology)

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