Premium
Antitumor activity of satraplatin in cisplatin‐resistant oral squamous cell carcinoma cells
Author(s) -
Yamano Yukio,
Shiiba Masashi,
Negoro Kenji,
Nakatani Ken,
Kasamatsu Atsushi,
Yamatoji Masanobu,
Sakuma Kentaro,
Ogoshi Kenji,
Iyoda Manabu,
Shinozuka Keiji,
Yokoe Hidetaka,
Wada Takeshi,
Fujita Shigeyuki,
Iwasawa Shunichiro,
Takiguchi Yuichi,
Tanzawa Hideki,
Uzawa Katsuhiro
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.21445
Subject(s) - cisplatin , clonogenic assay , cell culture , microbiology and biotechnology , chemistry , glutathione , cell , cancer research , mtt assay , flow cytometry , population , viability assay , biology , medicine , chemotherapy , biochemistry , enzyme , genetics , environmental health
Background. The aim of the current study was to identify the antitumor activity of satraplatin in paired cisplatin (CDDP)‐resistant oral squamous cell carcinoma (OSCC) cell line and its parental cell line.Methods. CDDP‐resistant (KB‐R) cells and parental cells (KB) pair were used. Viability was assessed using the MTT and clonogenic assay. Real‐time polymerase chain reaction (PCR), glutathione (GSH) assay, and flow cytometric analysis were used for further assessment.Results. KB‐R cells did not show cross‐resistance to satraplatin. The expression status of almost all transporters was upregulated in the KB‐R cells. There was no difference in the GSH levels between the KB and KB‐R cells. Flow cytometric analysis indicated that with satraplatin the G2/M phase was arrested in the KB‐R cells. KB‐R cells contain enriched side population cells.Conclusion. These data suggested that satraplatin has antitumor activity against the CDDP‐resistant OSCC cells. The mechanism of cross‐resistance to platinum agents seems to be multifactorial. © 2010 Wiley Periodicals, Inc. Head Neck, 2010