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Start Over Author "Shiow Lin Pan" Journal journal of biomedical science
5 results on '"Shiow Lin Pan"'

1. Inhibition of ras-mediated cell proliferation by benzyloxybenzaldehyde

Author

Shiow-Lin Pan, Jih-Hwa Guh, Ying-Wen Huang, Ya-Ling Chang, Chiung-Yun Chang, Li-Jiau Huang, Sheng-Chu Kuo, and Che-Ming Teng

Subjects
Dose-Response Relationship, Drug, MAP Kinase Signaling System, Endocrinology, Diabetes and Metabolism, Biochemistry (medical), Clinical Biochemistry, NF-kappa B, Antineoplastic Agents, Cell Biology, General Medicine, Muscle, Smooth, Vascular, Rats, Transcription Factor AP-1, Benzaldehydes, ras Proteins, Animals, Pharmacology (medical), Genes, Immediate-Early, Molecular Biology, Aorta, Cell Division
Abstract

Excessive proliferation of vascular smooth muscle cells (VSMC) in the intima is an important etiologic factor in vascular proliferative disorders such as atherosclerosis and restenosis after balloon angioplasty. Therefore, control of VSMC growth may be a suitable therapeutic intervention in vascular proliferative disorders. In the present work, we have studied the 2-benzyloxybenzaldehyde (CCY1a)-mediated antiproliferative effect and its mechanisms of action. CCY1a inhibited serum-induced VSMC proliferation in a concentration-dependent manner, as demonstrated using [(3)H]thymidine incorporation and MTT assays; the IC(50) values were calculated to be 7.0 x 10(-6) and 1.2 x 10(-5) M, respectively. Furthermore, it also significantly suppressed serum-induced progression of the cell cycle, as shown by flow cytometric analysis. CCY1a as well as PD98059 almost completely abolished serum-induced activation of p42/44 mitogen-activated protein kinase (MAPK), the downstream effectors of c-fos and c-jun mRNA expression and activator protein-1 (AP-1) DNA binding activity, suggesting the central roles of these signaling cascades. Interestingly, CCY1a also effectively blocked serum-induced Ikappa B-alpha phosphorylation, Ikappa B-alpha degradation and nuclear factor-kappa B (NF-kappa B) binding activity. Based on these observations, we examined the effect of CCY1a on serum-mediated Ras activity, an upstream regulator of the above signaling events. The data demonstrated a marked inhibition of Ras activation by CCY1a. We conclude that CCY1a blocks cell proliferation via inhibition of the upstream effector of Ras and downstream events, including p42/44 MAPK activation and c-fos and c-jun mRNA expression, as well as NF-kappa B and AP-1 DNA binding activities.

Published
2002
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2. Contents Vol. 9, 2002

Author

Hiraku Umemoto, Liangmei He, Ya-Ling Chang, Mei-Chiao Wu, Chi-Hung Lin, H. Yee, Tatsuo Muramatsu, Tohru Ibi, Fernando Augusto Proietti, Hsiu-Yu Lai, Koichi Furukawa, Shin-ichi Muramatsu, Binh N. Tran, Alice Y.W. Chang, Hung-Chou Kuo, Hung-Ming Chen, Imaharu Nakano, Wen-Fang Cheng, Shiow-Lin Pan, Chungming Chang, Kumi Nishizawa, Harm-Jan Borgeld, Ren-Bin Tang, Young-Chau Liu, Hal F. Yee, S. Chan, Pisit Tangkijvanich, Andrew M. James, Jan M. Orenstein, Steven P. Tam, Yukihiro Akao, Chen-Che Chu, Jin-Lian Tsai, Nobuko Ohishi, Elizabeth A. Rich, I. Bravo, May-Ghee Lum, Xavier Roucou, Paik-Seong Lim, Ta-Chen Lin, Chun-Ching Lin, J.A. Marshall, C.H. Lai, Samuel H.H. Chan, E. Gutiérrez-Reyes, Julie Y.H. Chan, Mei-Jie Jou, James K V Willson, Hsing I. Chen, Chuen Miin Leu, T.-C. Wu, Shigeaki Miyabayashi, Chia-Wei Liou, Pen-Hui Yin, Yueh-Mei Cheng, Che-Ming Teng, Fen-Hwa Wong, D.K.Y. Shum, Kunio Yagi, Catherine Transy, Jian-Sheng Gong, Keiya Ozawa, Horng-Der Shen, Ying-Wen Huang, Chai-Wei Liou, David Wang, Chien-Min Yang, Françoise Bergametti, Helen Wong, Sheng-Chu Kuo, June L. Traicoff, Y.S. Chan, Masayo Shamoto, J.-Y. Lee, Shuo-Bin Jou, Hong Chou, J.A. Moreno-Yanes, Stefanie N. Vogel, Keng-Fu Hsu, Anna Bárbara F. Carneiro-Proietti, M. Shehu-Xhilaga, S. Campbell, J. Mak, Hsin-Chen Lee, M.S. Cho, Cheng-po Hu, Tania M. Hansen, Chiung-Yun Chang, Ming F. Tam, Herbert C. Morse rd, John S. Cowdery, Akihiko Kikuchi, R. Bonfante-Cabarcas, Miyuki Kurata, Shan-Chun Chen, Ru Ping Lee, Julie Bianchi, Ching-Yun Chang, Chien-Fu Hung, Yi-Shing Ma, Cheng-Feng Lee, Arin J. Schroeder, Makoto Yoneda, Bernadette Catalan-Soares, Yao-Chung Chuang, Sammy Saab, Tsung-I Peng, Ko Sahashi, Henry Chai, Sanford D. Markowitz, Hsin-Su Yu, Kuan-Teh Jeang, Makoto Naoi, Hua-Yew Cheng, Ching-jang Huang, Michael P. Murphy, C. Nello, Phillip Nagley, Noriyuki Fuku, Sara I. Pai, Tzu-Ling Chen, Wan-Shung Fong, Yau-Huei Wei, Chin-Wen Chi, Maria L.R. Lim, Andrew C. Melton, Jin Zhang, Morris Ling, Yoshiji Yamada, Mary Bradford, Li-Jiau Huang, S.M. Crowe, N.E. Loureiro Dos Santos, Masashi Tanaka, Wakako Maruyama, Chin-Chang Huang, Jih-Hwa Guh, and Nien Tsung Lin

Subjects
Endocrinology, Diabetes and Metabolism, Biochemistry (medical), Clinical Biochemistry, Pharmacology (medical), Cell Biology, General Medicine, Molecular Biology
Published
2002
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3. Subject Index Vol. 9, 2002

Author

Young-Chau Liu, Michael P. Murphy, C. Nello, S. Campbell, Cheng-po Hu, Chiung-Yun Chang, Shin-ichi Muramatsu, Pisit Tangkijvanich, John S. Cowdery, Hal F. Yee, Jan M. Orenstein, Phillip Nagley, Hung-Ming Chen, J.A. Moreno-Yanes, Anna Bárbara F. Carneiro-Proietti, M. Shehu-Xhilaga, Chen-Che Chu, M.S. Cho, Bernadette Catalan-Soares, Paik-Seong Lim, Tatsuo Muramatsu, Morris Ling, Fernando Augusto Proietti, Steven P. Tam, T.-C. Wu, Ren-Bin Tang, May-Ghee Lum, Chun-Ching Lin, Tsung-I Peng, Ko Sahashi, Henry Chai, Sanford D. Markowitz, Shuo-Bin Jou, Akihiko Kikuchi, Chi-Hung Lin, Tohru Ibi, H. Yee, Li-Jiau Huang, Pen-Hui Yin, C.H. Lai, Chin-Chang Huang, Jih-Hwa Guh, S. Chan, Andrew M. James, Nien Tsung Lin, Keng-Fu Hsu, Shiow-Lin Pan, Nobuko Ohishi, Elizabeth A. Rich, Samuel H.H. Chan, J.A. Marshall, Julie Y.H. Chan, Hsing I. Chen, Ying-Wen Huang, Jin-Lian Tsai, I. Bravo, Mei-Jie Jou, Chuen Miin Leu, Hsiu-Yu Lai, Noriyuki Fuku, Sara I. Pai, Hung-Chou Kuo, Tania M. Hansen, Xavier Roucou, Chungming Chang, Shan-Chun Chen, Ru Ping Lee, Imaharu Nakano, Fen-Hwa Wong, Ta-Chen Lin, Catherine Transy, Kuan-Teh Jeang, Wen-Fang Cheng, Yao-Chung Chuang, S.M. Crowe, Chien-Fu Hung, R. Bonfante-Cabarcas, Chai-Wei Liou, E. Gutiérrez-Reyes, Horng-Der Shen, Françoise Bergametti, Chien-Min Yang, Herbert C. Morse rd, Masayo Shamoto, Helen Wong, Sheng-Chu Kuo, Y.S. Chan, Julie Bianchi, Ching-jang Huang, Koichi Furukawa, Ching-Yun Chang, Ming F. Tam, Kumi Nishizawa, Harm-Jan Borgeld, Hiraku Umemoto, Yi-Shing Ma, Binh N. Tran, Alice Y.W. Chang, Stefanie N. Vogel, Hsin-Su Yu, Shigeaki Miyabayashi, Jian-Sheng Gong, Makoto Naoi, Hua-Yew Cheng, Wan-Shung Fong, Maria L.R. Lim, Liangmei He, Chin-Wen Chi, Wakako Maruyama, Jin Zhang, Tzu-Ling Chen, Yau-Huei Wei, Mary Bradford, Andrew C. Melton, Ya-Ling Chang, David Wang, Kunio Yagi, Mei-Chiao Wu, Chia-Wei Liou, June L. Traicoff, Yueh-Mei Cheng, Che-Ming Teng, Yukihiro Akao, James K V Willson, Hong Chou, J. Mak, Sammy Saab, Masashi Tanaka, D.K.Y. Shum, Keiya Ozawa, Cheng-Feng Lee, Arin J. Schroeder, J.-Y. Lee, Hsin-Chen Lee, Miyuki Kurata, Makoto Yoneda, Yoshiji Yamada, and N.E. Loureiro Dos Santos

Subjects
Index (economics), Endocrinology, Diabetes and Metabolism, Biochemistry (medical), Clinical Biochemistry, Statistics, Pharmacology (medical), Subject (documents), Cell Biology, General Medicine, Molecular Biology, Mathematics
Published
2002
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4. Apoptosis signal-regulating kinase 1 mediates denbinobin-induced apoptosis in human lung adenocarcinoma cells.

Author

Chen-Tzu Kuo, Bing-Chang Chen, Chung-Chi Yu, Chih-Ming Weng, Ming-Jen Hsu, Chien-Chih Chen, Mei-Chieh Chen, Che-Ming Teng, Shiow-Lin Pan, Mauo-Ying Bien, Chung-Hung Shih, and Chien- Huang Lin

Subjects
APOPTOSIS, ANTIOXIDANTS, CHEMICAL inhibitors, ADENOCARCINOMA, PHOSPHORYLATION
Abstract

In the present study, we explore the role of apoptosis signal-regulating kinase 1 (ASK1) in denbinobin-induced apoptosis in human lung adenocarcinoma (A549) cells. Denbinobin-induced cell apoptosis was attenuated by an ASK1 dominant-negative mutant (ASK1DN), two antioxidants (N-acetyl-L-cysteine (NAC) and glutathione (GSH)), a c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and an activator protein-1 (AP-1) inhibitor (curcumin). Treatment of A549 cells with denbinobin caused increases in ASK1 activity and reactive oxygen species (ROS) production, and these effects were inhibited by NAC and GSH. Stimulation of A549 cells with denbinobin caused JNK activation; this effect was markedly inhibited by NAC, GSH, and ASK1DN. Denbinobin induced c-Jun phosphorylation, the formation of an AP-1-specific DNA-protein complex, and Bim expression. Bim knockdown using a bim short interfering RNA strategy also reduced denbinobininduced A549 cell apoptosis. The denbinobin-mediated increases in c-Jun phosphorylation and Bim expression were inhibited by NAC, GSH, SP600125, ASK1DN, JNK1DN, and JNK2DN. These results suggest that denbinobin might activate ASK1 through ROS production to cause JNK/AP-1 activation, which in turn induces Bim expression, and ultimately results in A549 cell apoptosis. [ABSTRACT FROM AUTHOR]

Published
2009
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5. Apoptosis signal-regulating kinase 1 mediates denbinobin-induced apoptosis in human lung adenocarcinoma cells

Author

Che-Ming Teng, Chung Chi Yu, Mauo Ying Bien, Chih Ming Weng, Chien-Huang Lin, Bing Chang Chen, Chien Chih Chen, Chung Hung Shih, Chen Tzu Kuo, Shiow Lin Pan, Mei Chieh Chen, and Ming Jen Hsu

Subjects
Small interfering RNA, Programmed cell death, Lung Neoplasms, Endocrinology, Diabetes and Metabolism, Clinical Biochemistry, lcsh:Medicine, Anthraquinones, Antineoplastic Agents, Apoptosis, Biology, Adenocarcinoma, MAP Kinase Kinase Kinase 5, Cell Line, Tumor, Humans, ASK1, Pharmacology (medical), Molecular Biology, A549 cell, chemistry.chemical_classification, Biochemistry, medical, Reactive oxygen species, Cell Death, Kinase, Research, Biochemistry (medical), lcsh:R, General Medicine, Cell Biology, Phenanthrenes, Cell biology, chemistry, Cell culture, Cancer research, Reactive Oxygen Species
Abstract

In the present study, we explore the role of apoptosis signal-regulating kinase 1 (ASK1) in denbinobin-induced apoptosis in human lung adenocarcinoma (A549) cells. Denbinobin-induced cell apoptosis was attenuated by an ASK1 dominant-negative mutant (ASK1DN), two antioxidants (N-acetyl-L-cysteine (NAC) and glutathione (GSH)), a c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and an activator protein-1 (AP-1) inhibitor (curcumin). Treatment of A549 cells with denbinobin caused increases in ASK1 activity and reactive oxygen species (ROS) production, and these effects were inhibited by NAC and GSH. Stimulation of A549 cells with denbinobin caused JNK activation; this effect was markedly inhibited by NAC, GSH, and ASK1DN. Denbinobin induced c-Jun phosphorylation, the formation of an AP-1-specific DNA-protein complex, and Bim expression. Bim knockdown using a bim short interfering RNA strategy also reduced denbinobin-induced A549 cell apoptosis. The denbinobin-mediated increases in c-Jun phosphorylation and Bim expression were inhibited by NAC, GSH, SP600125, ASK1DN, JNK1DN, and JNK2DN. These results suggest that denbinobin might activate ASK1 through ROS production to cause JNK/AP-1 activation, which in turn induces Bim expression, and ultimately results in A549 cell apoptosis.

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