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1. Silencing of Polo-Like Kinase (Plk) 1 via siRNA Causes Inhibition of Growth and Induction of Apoptosis in Human Esophageal Cancer Cells

Author

Quanhai Li, Youquan Bu, Fangzhou Song, and Zhengmei Yang

Subjects
Cancer Research, Small interfering RNA, Esophageal Neoplasms, Blotting, Western, Fluorescent Antibody Technique, Mitosis, Apoptosis, Cell Cycle Proteins, Polo-like kinase, Protein Serine-Threonine Kinases, Biology, Transfection, PLK1, Proto-Oncogene Proteins, Tumor Cells, Cultured, medicine, Humans, Gene Silencing, RNA, Messenger, RNA, Small Interfering, Mitotic cell cycle arrest, Mitotic catastrophe, Cell Proliferation, Cytokinesis, Reverse Transcriptase Polymerase Chain Reaction, Cell Cycle, Cancer, Genetic Therapy, General Medicine, Cell cycle, Flow Cytometry, medicine.disease, Oncology, Immunology, Cancer research, Sister Chromatid Exchange
Abstract

Esophageal cancer ranks among one of the most frequent causes of cancer death in the world. Polo-like kinase 1 (Plk1) is overexpressed in human tumors and has prognostic value in many cancers including esophageal cancer, indicating its potential as a therapeutic target. In this study, we investigated the therapeutic potential of Plk1 in esophageal cancer using the technique of RNA silencing via small interfering RNA (siRNA). Synthetic siRNA duplexes against Plk1 were introduced into 4 esophageal cancer cell lines, which subsequently resulted in a significant inhibition in Plk1 expression in the cells. We found that the targeted depletion of Plk1 caused a dramatic mitotic catastrophe (mitotic cell cycle arrest as well as defects in several mitotic events such as incomplete separation of sister chromatids and failure of cytokinesis) followed by massive apoptotic cell death, and eventually resulted in a significant decrease in growth and viability of all 4 esophageal cancer cell lines studied. In addition, our results also indicated that the mitotic arrest induced by Plk1 depletion is mediated by the inactivation of the cdc2/cyclin B1 complex. Taken together, our study strongly suggests that Plk1 may serve as a potential therapeutic target in human esophageal cancer.

Published
2008

2. Contents Vol. 74, 2008

Author

Goetz von Wichert, Dong Wook Shin, Bin Zhou, Hai-Yi Liu, J. Fiore, Giario Conti, Bing Xu, Lie Yang, Sergio Ricci, Kenji Sugamura, Zhengmei Yang, Stefan Breitenstein, Yong Chul Kwon, Davide Radice, Franco Nolè, Sang Yoon Park, Stefan Bierer, Stefan Dold, I. Floriani, Edwin Herrmann, Hidenori Akaike, Yoshiki Mizukami, Yuan Li, M. Medici, Bernhard C. Pestalozzi, Xiao-Gang Shen, Christoph Renner, Bonnie L. Hylander, Koji Kono, Joo-Hyun Nam, C. Marenghi, C. Codecà, F. Gray, M. Polivka, John F. Gibbs, Lothar Hertle, Masaharu Kasai, Quanhai Li, Yu-Fei Jiao, Alan Belicha-Villanueva, Osamu Muto, Laura Adamoli, Kohei Shitara, Chiara Catania, P. Bertheau, J.-M. Molina, Antonio Manganelli, Alessandra Rubagotti, Youquan Bu, D. Ferrari, Peter Kestenholz, Thomas Seufferlein, Elena Verri, Kousaku Mimura, L. Calabrese, Hamdy A. Azim, Chris Andrews, J.-B. Thiebault, Thomas Köpke, Frank Stenner-Liewen, Alberto Lapini, Zong-Guang Zhou, D. Alterio, Panagiotis Samaras, Francesco Boccardo, Noriyuki Yamada, Hidemitsu Sugai, M. Lagrange-Xelot, Julia Braun, Yuh Sakata, P. Foa, Jun-Min Song, Xiao-Feng Sun, Christian Wülfing, Giorgio Cruciani, Sang Min Park, Tamotsu Sugai, Young Ho Yun, Guido Adler, F. Chiesa, Yoshihiko Kawaguchi, Chong Taik Park, Filippo de Braud, Wataru Habano, B. Zuber, Volker Kaechele, Ling Wang, Hideki Fujii, B.A. Jereczek-Fossa, Yu-Jian Zeng, Elizabeth A. Repasky, Michele Battaglia, Fangzhou Song, Hatem A. Azim, Humberto Villavicencio, Aron Goldhirsch, Joachim Gerss, S. Gallien, A. Luciani, Alexander Imhof, Pablo Maroto Rey, Duk-Soo Bae, Jong Min Lee, Rong Wang, Shin-ichi Nakamura, R. Orecchia, Chi-Heum Cho, Tommaso De Pas, and Masaki Munakata

Subjects
Cancer Research, Oncology, General Medicine
Published
2008

3. Subject Index Vol. 74, 2008

Author

Hatem A. Azim, Osamu Muto, B.A. Jereczek-Fossa, Panagiotis Samaras, Bernhard C. Pestalozzi, Duk-Soo Bae, Noriyuki Yamada, Xiao-Gang Shen, C. Marenghi, Hai-Yi Liu, Francesco Boccardo, J.-B. Thiebault, Yuh Sakata, Lothar Hertle, Christoph Renner, Quanhai Li, Aron Goldhirsch, Shin-ichi Nakamura, M. Lagrange-Xelot, Jun-Min Song, Giario Conti, Lie Yang, Jong Min Lee, Xiao-Feng Sun, Zhengmei Yang, Hamdy A. Azim, Volker Kaechele, Rong Wang, Antonio Manganelli, Bing Xu, A. Luciani, Bin Zhou, J. Fiore, Alberto Lapini, Pablo Maroto Rey, R. Orecchia, Youquan Bu, Yuan Li, Kenji Sugamura, Bonnie L. Hylander, Christian Wülfing, Yu-Jian Zeng, Chris Andrews, I. Floriani, Hidenori Akaike, Alexander Imhof, Edwin Herrmann, Guido Adler, Chi-Heum Cho, Elizabeth A. Repasky, Michele Battaglia, Masaharu Kasai, Tommaso De Pas, Sang Min Park, Kohei Shitara, Fangzhou Song, Hideki Fujii, Julia Braun, D. Ferrari, Chiara Catania, Elena Verri, Humberto Villavicencio, Yoshihiko Kawaguchi, Davide Radice, Young Ho Yun, Wataru Habano, B. Zuber, F. Chiesa, Goetz von Wichert, Ling Wang, Chong Taik Park, Stefan Dold, M. Polivka, John F. Gibbs, Yoshiki Mizukami, Joachim Gerss, S. Gallien, F. Gray, Alan Belicha-Villanueva, Joo-Hyun Nam, Yu-Fei Jiao, Dong Wook Shin, Yong Chul Kwon, Sergio Ricci, Franco Nolè, Sang Yoon Park, Thomas Köpke, Frank Stenner-Liewen, Kousaku Mimura, D. Alterio, Filippo de Braud, Hidemitsu Sugai, Thomas Seufferlein, C. Codecà, Laura Adamoli, P. Bertheau, Alessandra Rubagotti, Tamotsu Sugai, Stefan Bierer, M. Medici, Peter Kestenholz, Zong-Guang Zhou, J.-M. Molina, L. Calabrese, Stefan Breitenstein, Koji Kono, Masaki Munakata, P. Foa, and Giorgio Cruciani

Subjects
Cancer Research, Index (economics), Oncology, Statistics, Subject (documents), General Medicine, Mathematics
Published
2008

4. Silencing of Polo-Like Kinase (Plk) 1 via siRNA Causes Inhibition of Growth and Induction of Apoptosis in Human Esophageal Cancer Cells.

Author

Youquan Bu, Zhengmei Yang, Quanhai Li, and Fangzhou Song

Subjects
*ESOPHAGEAL cancer, *PROTEIN kinases, *GENE silencing, *CELL cycle, *APOPTOSIS
Abstract

Esophageal cancer ranks among one of the most frequent causes of cancer death in the world. Polo-like kinase 1 (Plk1) is overexpressed in human tumors and has prognostic value in many cancers including esophageal cancer, indicating its potential as a therapeutic target. In this study, we investigated the therapeutic potential of Plk1 in esophageal cancer using the technique of RNA silencing via small interfering RNA (siRNA). Synthetic siRNA duplexes against Plk1 were introduced into 4 esophageal cancer cell lines, which subsequently resulted in a significant inhibition in Plk1 expression in the cells. We found that the targeted depletion of Plk1 caused a dramatic mitotic catastrophe (mitotic cell cycle arrest as well as defects in several mitotic events such as incomplete separation of sister chromatids and failure of cytokinesis) followed by massive apoptotic cell death, and eventually resulted in a significant decrease in growth and viability of all 4 esophageal cancer cell lines studied. In addition, our results also indicated that the mitotic arrest induced by Plk1 depletion is mediated by the inactivation of the cdc2/cyclin B1 complex. Taken together, our study strongly suggests that Plk1 may serve as a potential therapeutic target in human esophageal cancer. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2008
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