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

Yukio Yamano; 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

doi:10.1002/hed.21445

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

Yukio Yamano, 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

Research output: Contribution to journal › Article › peer-review

5 Citations (Scopus)

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.

Original language	English
Pages (from-to)	309-317
Number of pages	9
Journal	Head and Neck
Volume	33
Issue number	3
DOIs	https://doi.org/10.1002/hed.21445
Publication status	Published - Mar 2011
Externally published	Yes

Keywords

cisplatin
cross-resistance
drug resistance
satraplatin
side population

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10.1002/hed.21445

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Yamano, Y., Shiiba, M., Negoro, K., Nakatani, K., Kasamatsu, A., Yamatoji, M., Sakuma, K., Ogoshi, K., Iyoda, M., Shinozuka, K., Yokoe, H., Wada, T., Fujita, S., Iwasawa, S., Takiguchi, Y., Tanzawa, H., & Uzawa, K. (2011). Antitumor activity of satraplatin in cisplatin-resistant oral squamous cell carcinoma cells. Head and Neck, 33(3), 309-317. https://doi.org/10.1002/hed.21445

@article{8ec45220dc304b3493d93a17e9a2744c,

title = "Antitumor activity of satraplatin in cisplatin-resistant oral squamous cell carcinoma cells",

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.",

keywords = "cisplatin, cross-resistance, drug resistance, satraplatin, side population",

author = "Yukio Yamano and Masashi Shiiba and Kenji Negoro and Ken Nakatani and Atsushi Kasamatsu and Masanobu Yamatoji and Kentaro Sakuma and Kenji Ogoshi and Manabu Iyoda and Keiji Shinozuka and Hidetaka Yokoe and Takeshi Wada and Shigeyuki Fujita and Shunichiro Iwasawa and Yuichi Takiguchi and Hideki Tanzawa and Katsuhiro Uzawa",

year = "2011",

month = mar,

doi = "10.1002/hed.21445",

language = "English",

volume = "33",

pages = "309--317",

journal = "Head and Neck",

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publisher = "John Wiley & Sons Inc.",

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Yamano, Y, Shiiba, M, Negoro, K, Nakatani, K, Kasamatsu, A, Yamatoji, M, Sakuma, K, Ogoshi, K, Iyoda, M, Shinozuka, K, Yokoe, H, Wada, T, Fujita, S, Iwasawa, S, Takiguchi, Y, Tanzawa, H & Uzawa, K 2011, 'Antitumor activity of satraplatin in cisplatin-resistant oral squamous cell carcinoma cells', Head and Neck, vol. 33, no. 3, pp. 309-317. https://doi.org/10.1002/hed.21445

TY - JOUR

T1 - Antitumor activity of satraplatin in cisplatin-resistant oral squamous cell carcinoma cells

AU - Yamano, Yukio

AU - Shiiba, Masashi

AU - Negoro, Kenji

AU - Nakatani, Ken

AU - Kasamatsu, Atsushi

AU - Yamatoji, Masanobu

AU - Sakuma, Kentaro

AU - Ogoshi, Kenji

AU - Iyoda, Manabu

AU - Shinozuka, Keiji

AU - Yokoe, Hidetaka

AU - Wada, Takeshi

AU - Fujita, Shigeyuki

AU - Iwasawa, Shunichiro

AU - Takiguchi, Yuichi

AU - Tanzawa, Hideki

AU - Uzawa, Katsuhiro

PY - 2011/3

Y1 - 2011/3

N2 - 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.

AB - 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.

KW - cisplatin

KW - cross-resistance

KW - drug resistance

KW - satraplatin

KW - side population

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U2 - 10.1002/hed.21445

DO - 10.1002/hed.21445

M3 - Article

C2 - 20848452

AN - SCOPUS:79951717852

SN - 1043-3074

VL - 33

SP - 309

EP - 317

JO - Head and Neck

JF - Head and Neck

IS - 3

ER -

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

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