Suberoylanilide hydroxamic acid (SAHA) induces apoptosis or autophagy-associated cell death in chondrosarcoma cell lines

Shunsaku Yamamoto, Kazuhiro Tanaka, Riku Sakimura, Takamitsu Okada, Tomoyuki Nakamura, Yan Li, Minoru Takasaki, Yusaku Nakabeppu, Yukihide Iwamoto

Research output: Contribution to journalArticle

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Abstract

Background: Since chondrosarcoma has a high resistance to conventional chemotherapy and radiotherapy, surgical resection is currently the only effective treatment. Histone deacetylase (HDAC) inhibitor exert anticancer effects, but have not been tested in chondrosarcoma. Materials and Methods: We investigated the phenotypic change in chondrosarcoma cells treated with SAHA by cell viability assay, Western blot, flow cytometric analysis and electron microscopy. Results: SAHA inhibited the growth of chondrosarcoma cell lines and induced apoptosis in SW1353 with a cleaved-PARP expression and sub-G1 fragmentation according to flow cytometric analysis. On the other hand, in RCS and OUMS-27, SAHA induced autophagy-associated cell death as shown by the detection of autophagosome-specific protein and specific ultrastructural morphology in the cytoplasm. In addition, SAHA significantly inhibited tumor growth in an in vivo xenograft model. Conclusion: These results suggest that SAHA might be a promising agent for performing clinically useful chemotherapy against chondrosarcomas.

Original languageEnglish
Pages (from-to)1585-1591
Number of pages7
JournalAnticancer research
Volume28
Issue number3 A
Publication statusPublished - May 1 2008

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Chondrosarcoma
Autophagy
Cell Death
Apoptosis
Cell Line
Drug Therapy
Histone Deacetylase Inhibitors
Growth
Heterografts
Cell Survival
Electron Microscopy
Cytoplasm
Radiotherapy
Western Blotting
vorinostat
Neoplasms
Proteins

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Yamamoto, S., Tanaka, K., Sakimura, R., Okada, T., Nakamura, T., Li, Y., ... Iwamoto, Y. (2008). Suberoylanilide hydroxamic acid (SAHA) induces apoptosis or autophagy-associated cell death in chondrosarcoma cell lines. Anticancer research, 28(3 A), 1585-1591.

Suberoylanilide hydroxamic acid (SAHA) induces apoptosis or autophagy-associated cell death in chondrosarcoma cell lines. / Yamamoto, Shunsaku; Tanaka, Kazuhiro; Sakimura, Riku; Okada, Takamitsu; Nakamura, Tomoyuki; Li, Yan; Takasaki, Minoru; Nakabeppu, Yusaku; Iwamoto, Yukihide.

In: Anticancer research, Vol. 28, No. 3 A, 01.05.2008, p. 1585-1591.

Research output: Contribution to journalArticle

Yamamoto, S, Tanaka, K, Sakimura, R, Okada, T, Nakamura, T, Li, Y, Takasaki, M, Nakabeppu, Y & Iwamoto, Y 2008, 'Suberoylanilide hydroxamic acid (SAHA) induces apoptosis or autophagy-associated cell death in chondrosarcoma cell lines', Anticancer research, vol. 28, no. 3 A, pp. 1585-1591.
Yamamoto S, Tanaka K, Sakimura R, Okada T, Nakamura T, Li Y et al. Suberoylanilide hydroxamic acid (SAHA) induces apoptosis or autophagy-associated cell death in chondrosarcoma cell lines. Anticancer research. 2008 May 1;28(3 A):1585-1591.
Yamamoto, Shunsaku ; Tanaka, Kazuhiro ; Sakimura, Riku ; Okada, Takamitsu ; Nakamura, Tomoyuki ; Li, Yan ; Takasaki, Minoru ; Nakabeppu, Yusaku ; Iwamoto, Yukihide. / Suberoylanilide hydroxamic acid (SAHA) induces apoptosis or autophagy-associated cell death in chondrosarcoma cell lines. In: Anticancer research. 2008 ; Vol. 28, No. 3 A. pp. 1585-1591.
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AU - Okada, Takamitsu

AU - Nakamura, Tomoyuki

AU - Li, Yan

AU - Takasaki, Minoru

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AB - Background: Since chondrosarcoma has a high resistance to conventional chemotherapy and radiotherapy, surgical resection is currently the only effective treatment. Histone deacetylase (HDAC) inhibitor exert anticancer effects, but have not been tested in chondrosarcoma. Materials and Methods: We investigated the phenotypic change in chondrosarcoma cells treated with SAHA by cell viability assay, Western blot, flow cytometric analysis and electron microscopy. Results: SAHA inhibited the growth of chondrosarcoma cell lines and induced apoptosis in SW1353 with a cleaved-PARP expression and sub-G1 fragmentation according to flow cytometric analysis. On the other hand, in RCS and OUMS-27, SAHA induced autophagy-associated cell death as shown by the detection of autophagosome-specific protein and specific ultrastructural morphology in the cytoplasm. In addition, SAHA significantly inhibited tumor growth in an in vivo xenograft model. Conclusion: These results suggest that SAHA might be a promising agent for performing clinically useful chemotherapy against chondrosarcomas.

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