2. Academic Validation
  3. Antitumor activity of satraplatin in cisplatin-resistant oral squamous cell carcinoma cells

Antitumor activity of satraplatin in cisplatin-resistant oral squamous cell carcinoma cells

  • Head Neck. 2011 Mar;33(3):309-17. doi: 10.1002/hed.21445.
Yukio Yamano 1,  Masashi Shiiba,  Kenji Negoro,  Ken Nakatani,  Atsushi Kasamatsu,  Masanobu Yamatoji,  Kentaro Sakuma,  Kenji Ogoshi,  Manabu Iyoda,  Keiji Shinozuka,  Hidetaka Yokoe,  Takeshi Wada,  Shigeyuki Fujita,  Shunichiro Iwasawa,  Yuichi Takiguchi,  Hideki Tanzawa,  Katsuhiro Uzawa
Affiliations

Affiliation

  • 1 Department of Clinical Molecular Biology, Graduate School of Medicine, Chiba University, Chiba, Japan.
PMID: 20848452 DOI: 10.1002/hed.21445
Abstract

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.

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