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Although salivary gland adenocarcinoma NOS accounts for third prevalence rate of all salivary gland tumors, it is one of the most aggressive solid tumors. Current therapy does not significantly improve survival rates. Thus, investigating new therapeutic modalities against salivary gland adenocarcinoma NOS is necessary. It is well known that docetaxel(TXT) as an antimicrotubulin agent induces mitotic block in proliferating cells. TXT has significant antitumor effects, and it is currently being tested in patients with malignant tumors, but TXT has not yet been tested in malignant salivary gland tumors. The purpose of this study were to examine the effects of TXT
and to evaluate the biological mechanisms of TXT on salivary gland adenocarcinoma NOS. Proliferation, cell cycle regulation, connexin43 expression, apoptosis, and Fas receptor(FasR) expression were measured in cultured SGT cell line. Proliferation was little changed after 10ng/ml TXT exposure, but cellular proliferation was inhibited according to increasing concentration of TXT and time. Especially it was
prominently inhibited after 96 hrs at 20ng/ml. G2-M arrest stage showed about up to 5 fold increase after exposure of TXT by flow cytometry. Apoptosis index showed about up to 8 fold increase after exposure of TXT by flow cytometry. Fas expression showed about up to 3 fold increase after exposure of TXT by flow cytometry. Apoptosis showed about up to 3 fold increase at 20ng/ml after exposure
of TXT and anti-Fas agonist by flow cytometry. In Immunoslot blotting, Cx 43 protein expression was increased after TXT treatment. It suggested that TXT might induce apoptosis in SGT cells and could be used as a potent and specific chemotherapeutic tool for the
treatment of salivary gland adenocarcinoma NOS in future.