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Tumor growth inhibition of metastatic nasopharyngeal carcinoma cell lines by low dose of arsenic trioxide via alteration of cell cycle progression and induction of apoptosis
Author(s) -
Yeh KunYun,
Chang John W.C.,
Li YingYing,
Wang ChengHsu,
Wang HungMing
Publication year - 2011
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.21535
Subject(s) - arsenic trioxide , nasopharyngeal carcinoma , apoptosis , in vivo , cancer research , cell cycle , cell cycle checkpoint , cell growth , medicine , primary tumor , cell culture , cancer , oncology , chemistry , metastasis , biology , radiation therapy , biochemistry , genetics , microbiology and biotechnology
Background. Although arsenic trioxide (ATO) has displayed anticancer activity against primary nasopharyngeal carcinoma (NPC), its efficacy in metastatic NPC deserved further investigation because the biological/therapeutic difference in cancer cells probably exists between primary and distant sites. Methods. Two human metastatic NPC cell lines (NPC‐BM1 and NPC‐BM2) were investigated. We measured cellular proliferation, cell cycle, and apoptotic extent of BM1 and BM2 cells treated with ATO in vitro. Furthermore, we evaluated the tumor growth after ATO treatment in vivo. Results. Low‐dose ATO treatment is sufficient to induce an antiproliferative effect, alter the cell cycle, and increase apoptosis in BM1 and BM2 cells. BM1 tumor growth in a xenograft model with low‐dose and short‐schedule (1 mg/kg/day, intraperitoneal injection for 5 consecutive days) of ATO treatment significantly slowed in vivo. Conclusion. ATO at low dose seems to be an encouraging schedule for palliative treatment of metastatic NPC. © 2010 Wiley Periodicals, Inc. Head Neck, 2011