Sulindac sulfide-induced apoptosis in sinonasal cancer cells

Chang-Hoon Kim, Kyoung Seob Song, Kyung Su Kim, Jin Young Kim, Bong Jae Lee, Jeung Gweon Lee, Joo Heon Yoon

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Conclusions. These results demonstrate that sulindac sulfide can induce cell death in maxillary cancer cells, and that sulindac sulfide-induced apoptosis is related to the extracellular signal-regulated kinase/p38 MAPK-caspase 3 signaling pathway. Objective. Head and neck cancer is the sixth commonest cancer in the human body. Squamous cell carcinoma accounts for most sinonasal cancers. However, little is known regarding the biochemical mechanism(s) of cell death in sinonasal cancers. Recently, human epidemiological and clinical intervention studies have indicated that sulindac, a non-steroidal anti-inflammatory drug, exhibits chemopreventive activity in colorectal cancer. In this study, we aimed to investigate whether sulindac sulfide can induce apoptosis in sinonasal cancer cells and what type of molecular mechanisms induces the death of sinonasal cancer cells. Material and methods. Sinonasal cancer cells (Asan Medical Center-Head and Neck Cancer 5) were treated with various concentrations of sulindac sulfide. The degree of cell death was determined by means of a fluorescence-activated cell scan and the signal transduction pathway for cell death was examined. Results. Human nasal cavity cancer cells treated with sulindac sulfide underwent cell death, and the induction of apoptosis occurred in a dose-dependent manner. Moreover, sulindac sulfide-induced apoptosis was abolished by treatment with the caspase inhibitor Z-VAD-fmk and the mitogen-activated protein kinase (MAPK) inhibitors PD98059 and SB203580.

Original languageEnglish
Pages (from-to)201-206
Number of pages6
JournalActa Oto-Laryngologica
Volume125
Issue number2
DOIs
Publication statusPublished - 2005 Mar 10

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Apoptosis
Cell Death
Neoplasms
Head and Neck Neoplasms
Nose Neoplasms
Sulindac
Caspase Inhibitors
Mitogen-Activated Protein Kinase 3
Nasal Cavity
Extracellular Signal-Regulated MAP Kinases
p38 Mitogen-Activated Protein Kinases
Protein Kinase Inhibitors
sulindac sulfide
Mitogen-Activated Protein Kinases
Human Body
Caspase 3
Squamous Cell Carcinoma
Colorectal Neoplasms
Signal Transduction
Anti-Inflammatory Agents

All Science Journal Classification (ASJC) codes

  • Otorhinolaryngology

Cite this

Kim, C-H., Song, K. S., Kim, K. S., Kim, J. Y., Lee, B. J., Lee, J. G., & Yoon, J. H. (2005). Sulindac sulfide-induced apoptosis in sinonasal cancer cells. Acta Oto-Laryngologica, 125(2), 201-206. https://doi.org/10.1080/00016480410020293
Kim, Chang-Hoon ; Song, Kyoung Seob ; Kim, Kyung Su ; Kim, Jin Young ; Lee, Bong Jae ; Lee, Jeung Gweon ; Yoon, Joo Heon. / Sulindac sulfide-induced apoptosis in sinonasal cancer cells. In: Acta Oto-Laryngologica. 2005 ; Vol. 125, No. 2. pp. 201-206.
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abstract = "Conclusions. These results demonstrate that sulindac sulfide can induce cell death in maxillary cancer cells, and that sulindac sulfide-induced apoptosis is related to the extracellular signal-regulated kinase/p38 MAPK-caspase 3 signaling pathway. Objective. Head and neck cancer is the sixth commonest cancer in the human body. Squamous cell carcinoma accounts for most sinonasal cancers. However, little is known regarding the biochemical mechanism(s) of cell death in sinonasal cancers. Recently, human epidemiological and clinical intervention studies have indicated that sulindac, a non-steroidal anti-inflammatory drug, exhibits chemopreventive activity in colorectal cancer. In this study, we aimed to investigate whether sulindac sulfide can induce apoptosis in sinonasal cancer cells and what type of molecular mechanisms induces the death of sinonasal cancer cells. Material and methods. Sinonasal cancer cells (Asan Medical Center-Head and Neck Cancer 5) were treated with various concentrations of sulindac sulfide. The degree of cell death was determined by means of a fluorescence-activated cell scan and the signal transduction pathway for cell death was examined. Results. Human nasal cavity cancer cells treated with sulindac sulfide underwent cell death, and the induction of apoptosis occurred in a dose-dependent manner. Moreover, sulindac sulfide-induced apoptosis was abolished by treatment with the caspase inhibitor Z-VAD-fmk and the mitogen-activated protein kinase (MAPK) inhibitors PD98059 and SB203580.",
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Kim, C-H, Song, KS, Kim, KS, Kim, JY, Lee, BJ, Lee, JG & Yoon, JH 2005, 'Sulindac sulfide-induced apoptosis in sinonasal cancer cells', Acta Oto-Laryngologica, vol. 125, no. 2, pp. 201-206. https://doi.org/10.1080/00016480410020293

Sulindac sulfide-induced apoptosis in sinonasal cancer cells. / Kim, Chang-Hoon; Song, Kyoung Seob; Kim, Kyung Su; Kim, Jin Young; Lee, Bong Jae; Lee, Jeung Gweon; Yoon, Joo Heon.

In: Acta Oto-Laryngologica, Vol. 125, No. 2, 10.03.2005, p. 201-206.

Research output: Contribution to journalArticle

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T1 - Sulindac sulfide-induced apoptosis in sinonasal cancer cells

AU - Kim, Chang-Hoon

AU - Song, Kyoung Seob

AU - Kim, Kyung Su

AU - Kim, Jin Young

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AU - Lee, Jeung Gweon

AU - Yoon, Joo Heon

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N2 - Conclusions. These results demonstrate that sulindac sulfide can induce cell death in maxillary cancer cells, and that sulindac sulfide-induced apoptosis is related to the extracellular signal-regulated kinase/p38 MAPK-caspase 3 signaling pathway. Objective. Head and neck cancer is the sixth commonest cancer in the human body. Squamous cell carcinoma accounts for most sinonasal cancers. However, little is known regarding the biochemical mechanism(s) of cell death in sinonasal cancers. Recently, human epidemiological and clinical intervention studies have indicated that sulindac, a non-steroidal anti-inflammatory drug, exhibits chemopreventive activity in colorectal cancer. In this study, we aimed to investigate whether sulindac sulfide can induce apoptosis in sinonasal cancer cells and what type of molecular mechanisms induces the death of sinonasal cancer cells. Material and methods. Sinonasal cancer cells (Asan Medical Center-Head and Neck Cancer 5) were treated with various concentrations of sulindac sulfide. The degree of cell death was determined by means of a fluorescence-activated cell scan and the signal transduction pathway for cell death was examined. Results. Human nasal cavity cancer cells treated with sulindac sulfide underwent cell death, and the induction of apoptosis occurred in a dose-dependent manner. Moreover, sulindac sulfide-induced apoptosis was abolished by treatment with the caspase inhibitor Z-VAD-fmk and the mitogen-activated protein kinase (MAPK) inhibitors PD98059 and SB203580.

AB - Conclusions. These results demonstrate that sulindac sulfide can induce cell death in maxillary cancer cells, and that sulindac sulfide-induced apoptosis is related to the extracellular signal-regulated kinase/p38 MAPK-caspase 3 signaling pathway. Objective. Head and neck cancer is the sixth commonest cancer in the human body. Squamous cell carcinoma accounts for most sinonasal cancers. However, little is known regarding the biochemical mechanism(s) of cell death in sinonasal cancers. Recently, human epidemiological and clinical intervention studies have indicated that sulindac, a non-steroidal anti-inflammatory drug, exhibits chemopreventive activity in colorectal cancer. In this study, we aimed to investigate whether sulindac sulfide can induce apoptosis in sinonasal cancer cells and what type of molecular mechanisms induces the death of sinonasal cancer cells. Material and methods. Sinonasal cancer cells (Asan Medical Center-Head and Neck Cancer 5) were treated with various concentrations of sulindac sulfide. The degree of cell death was determined by means of a fluorescence-activated cell scan and the signal transduction pathway for cell death was examined. Results. Human nasal cavity cancer cells treated with sulindac sulfide underwent cell death, and the induction of apoptosis occurred in a dose-dependent manner. Moreover, sulindac sulfide-induced apoptosis was abolished by treatment with the caspase inhibitor Z-VAD-fmk and the mitogen-activated protein kinase (MAPK) inhibitors PD98059 and SB203580.

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