tNOX is both necessary and sufficient as a cellular target for the
anticancer actions of capsaicin and the green tea catechin
(-)-epigallocatechin-3-gallate
Issue title: Papers from the 7th International Conference on
Plasma Redox Systems and their Role in Biological Stress and Disease
Affiliations: Department of Medicinal Chemistry and Molecular
Pharmacology, Purdue University, West Lafayette, IN 47907, USA | Department of Foods and Nutrition, Purdue University,
West Lafayette, IN 47907, USA
Note: [] Address for correspondence: Department of Medicinal Chemistry
and Molecular Pharmacology, 201 S. University Street, Purdue University, West
Lafayette, IN 47907-2064, USA. Tel.: +1 765 494 1388; Fax: +1 765 494-4007;
E-mail: morre@pharmacy.purdue.edu
Abstract: Capsaicin and the principal green tea catechin,
(-)-epigallocatechin-3-gallate (EGCg), target tNOX, a tumor (cancer)-specific
surface hydroquinone (NADH) oxidase with protein disulfide-thiol interchange
activity (ECTO-NOX protein). Accordingly vector-forced over expression of tNOX
in MCF-10A mammary epithelia or COS cells that lack tNOX or in COS cells that
underexpress tNOX enhanced the susceptibility of growth and apoptosis to both
EGCg and capsaicin. Additionally, the tNOX-transfected MCF-10A cells
proliferated in Matrigel, a measure of invasiveness. In contrast, oligomeric
antisense tNOX DNA abrogated growth inhibition by EGCg and capsaicin and
reduced anchorage-dependent growth of HeLa (human cervical carcinoma) cells
that naturally overexpress tNOX. The findings show cell surface expression of
tNOX as both necessary and sufficient for the cellular anticancer activities
attributed to both EGCg and capsaicin.
