Affiliations: Institute of Biomedical Sciences, National Chung Hsing
University, Taichung, 40227, Taiwan, Republic of China
Note: [] Address for correspondence: Dr. Pin Ju Chueh, Institute of
Biomedical Sciences, National Chung Hsing University, 250 Kuo-Kuang Rd.
Taichung, 40227, Taiwan, Republic of China. Tel.: +886 4 22840896 ext 120; Fax:
+886 4 22853469; E-mail: pjchueh@dragon.nchu.edu.tw
Abstract: Previous reports have described a tumor-associated NADH oxidase
(tNOX) and its continuous activation in transformed culture cells. Certain
anticancer drugs have been shown to inhibit preferentially both the tNOX
activity and the growth of transformed culture cells and the cytotoxicity is
associated with the induction of apoptosis. To investigate the biological
function of tNOX protein, we have raised polyclonal antisera against bacterial
expressed tNOX protein and the antisera are able to recognize protein bands in
transformed cells but not the non-transformed cells tested. With tNOX antisera
treatment, the survival in transformed cell lines is decreased but not the
non-transformed cells. In addition, tNOX antisera-induced cytotoxicity is
accompanied by the induction of apoptosis. However, slightly higher amount of
PARP cleavage and activation of caspase-9 are observed in tNOX antisera treated
HCT116 cells. Further experiments have demonstrated the activation of JNK and
phosphorylation of p53 by treatment. In addition, tNOX antisera treatment leads
to an impressive increase in reactive oxygen species in COS cells but not the
control sera. Our data suggest that (a) tNOX antisera treatment may inhibit the
growth of transformed cells by inducing apoptosis and (b) the apoptotic
mechanism might be through modulating ROS production and JNK pathway.
