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Effect of polyclonal antisera to recombinant tNOX protein on the growth of transformed cells
Author(s) -
Chen ChunFeng,
Huang Shing,
Liu ShanChi,
Chueh Pin Ju
Publication year - 2006
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520280206
Subject(s) - antiserum , polyclonal antibodies , apoptosis , cell culture , cytotoxicity , biology , recombinant dna , microbiology and biotechnology , in vitro , antibody , biochemistry , immunology , gene , genetics
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.