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2. Oncogenic Ras-Induced Morphologic Change Is through MEK/ERK Signaling Pathway to Downregulate Stat3 at a Posttranslational Level in NIH3T3 Cells

Author

Hsuan-Heng Yeh, Chin-Han Wu, Raghavaraju Giri, Ken Kato, Kimitoshi Kohno, Hiroto Izumi, Cheng-Yang Chou, Wu-Chou Su, and Hsiao-Sheng Liu

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Ras is a key regulator of the MAP kinase-signaling cascade and may cause morphologic change of Ras-transformed cells. Signal transducer and activator of transcription 3 (Stat3) can be activated by cytokine stimulation. In this study, we unravel that Ha-rasV12 overexpression can downregulate the expression of Stat3 protein at a posttranslational level in NIH3T3 cells. Furthermore, we demonstrate that Stat3 expression downregulated by Ha-rasV12 overexpression is through proteosome degradation and not through a mTOR/p70S6K-related signaling pathway. The suppression of Stat3 accompanied by the morphologic change induced by Ha-rasV12 was through mitogen extracellular kinase (MEK)/extracellular-regulated kinase (ERK) signaling pathway. Microtubule disruption is involved in Ha-rasV12-induced morphologic change, which could be reversed by overexpression of Stat3. Taken together, we are the first to demonstrate that Stat3 protein plays a critical role in Ha-rasV12-induced morphologic change. Oncogenic Ras-triggered morphologic change is through the activation of MEK/ERK to posttranslationally downregulate Stat3 expression. Our finding may shed light on developing novel therapeutic strategies against Ras-related tumorigenesis.

Published
2008
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3. Y-box binding protein-1 (YB-1) promotes cell cycle progression through CDC6-dependent pathway in human cancer cells

Author

Hiroto Izumi, Michihiko Kuwano, Mayumi Ono, Kosuke Watari, Kimitoshi Kohno, Shinji Ohno, Yuji Basaki, Takuya Kubo, Yuichi Murakami, Hidetoshi Kawaguchi, Fumihito Hosoi, Kenji Nakano, and Ken Ichi Taguchi

Subjects
Adult, Cancer Research, Adolescent, Cellular differentiation, Cyclin A, Breast Neoplasms, Cell Cycle Proteins, Biology, CDC6, YB-1, Young Adult, Japan, Biomarkers, Tumor, Humans, Aged, Cell Proliferation, Cyclin-dependent kinase 1, Cell growth, Cell Cycle, Nuclear Proteins, Middle Aged, Cell cycle, Cell biology, Oncology, Cancer cell, biology.protein, Cancer research, Female, Y-Box-Binding Protein 1, Cell cycle regulation, A431 cells, Restriction point
Abstract

Y-box binding protein-1 (YB-1) plays pivotal roles in acquisition of global drug resistance and cell growth promotion through transcriptional activation of genes for both drug resistance and growth factor receptors. In this study, we investigated whether YB-1 is involved in regulation of the cell cycle and cell proliferation of human cancer cells. Treatment with YB-1 siRNA caused a marked suppression of cell proliferation and expression of a cell cycle related gene, CDC6 by cancer cells. Of cell cycle of cancer cells, S phase content was specifically reduced by knockdown of YB-1. The overexpression of CDC6 abrogated this inhibition of both cell proliferation and S phase entry. ChIP assay demonstrated that YB-1 binds to a Y-box located in the promoter region of the CDC6 gene. Expression of cyclin D1, CDK1 and CDK2 was also reduced with increased expression of p21(Cip1) and p16(INK4A) when treated with YB-1 siRNA. Furthermore, the nuclear YB-1 expression was significantly associated with the level of CDC6 nuclear expression in patients with breast cancer. In conclusion, YB-1 plays an important role in cell cycle progression at G1/S of human cancer cells. YB-1 thus could be a potent biomarker for tumour growth and cell cycle in its close association with CDC6.

Published
2010

4. Contributors

Author

Winsome Abbott-Johnson, Niyazi Acar, Vaishali Agte, Daniel Agudelo, Maria Antonietta Altea, R.A. Armstrong, Tin Aung, Bahri Aydın, Fereshteh Bahmani, D. Balmer, S. Zahra Bathaie, Lynne Bell, Tos T.J.M. Berendschot, Paul S. Bernstein, Brian M. Besch, Philippe Bourassa, R.B. Bozard, Lionel Bretillon, Alain M. Bron, Benjamin Buaud, Gabriëlle H.S. Buitendijk, Laurie T. Butler, Aldo Caporossi, Stefano Caragiuli, Chloé Cartier, Cristina Cartiglia, Chi-Ming Chan, Min-Lee Chang, Bashira A. Charles, Emily Y. Chew, Ching-Yu Cheng, Chung-Jung Chiu, Deepika Chopra, Patricia Coelho de Velasco, David Coman, Nicole Combe, Dolores Corella, M. Cossenza, Simonetta Costa, Catherine P. Creuzot-Garcher, Maria Cristina de Oliveira Izar, R.P. Cubbidge, Alyssa Cwanger, Cécile Delcourt, Marie-Noëlle Delyfer, I.C.L. Domith, David Dunaief, Joshua L. Dunaief, Rajan Elanchezhian, Andrew W. Eller, T.G. Encarnação, Mesut Erdurmuş, Evangelina Espósito, Asghar Farajzadeh, David T. Field, Silvia C. Finnemann, Steven J. Fliesler, Nicolas Froger, P.S. Ganapathy, V. Ganapathy, Jose J. Garcia-Medina, Pitchairaj Geraldine, Carmen Giannantonio, C.R. Gibson, Snehal Gite, N. Goldenberg-Cohen, Glen Gole, Ian R. Gorovoy, Julia A. Haller, Lisa Hark, Rijo Hayashi, Hui He, Tatiana Helfenstein, Francisco Antonio Helfenstein Fonseca, Ken-ichi Hosoya, Yi-Ling Huang, Chi-Feng Hung, M. Ibberson, Hiroto Izumi, Alberto Izzotti, Riikka L. Järvinen, Hua Ji, Yao Jin, Corinne Joffre, Choun-Ki Joo, Sang Hoon Jung, Heikki P. Kallio, Paul Kerlin, Eun Chul Kim, Jin Sook Kim, Amar U. Kishan, Caroline C.W. Klaver, Kimitoshi Kohno, Jean-François Korobelnik, Yoshiyuki Kubo, Petra S. Larmo, Ryszard Lauterbach, Ling-Jun Li, Dingbo Lin, M.I. Lopez-Galvez, Yi Lu, Zhi-Quan Lu, F. Manco Lavado, Claudio Marcocci, Shilpa Mathew, Cosimo Mazzotta, Francesca Menconi, Naoya Miyamoto, Bobeck S. Modjtahedi, Lawrence S. Morse, Sarah W. Mount, Arumugam R. Muralidharan, Benjamin P. Nicholson, R. Paes-de-Carvalho, J.C. Pastor, Dorota Pawlik, John F. Payne, Daniel Petrovič, Serge Picaud, Maria D. Pinazo-Duran, Adela Mariana Pintea, Jogchum Plat, C.C. Portugal, Ananda S. Prasad, Victor R. Preedy, Jiang Qin, R. Roduit, Costantino Romagnoli, Marie-Bénédicte Rougier, Dumitriţa Olivia Rugină, Charumathi Sabanayagam, Sergio Claudio Saccà, José-Alain Sahel, Dave Saint-Amour, Pedro Sanz-Solana, Seang Mei Saw, D.F. Schorderet, Claudio Alberto Serfaty, Horacio M. Serra, Saumil Sethna, Jay Siak, Hüseyin Simavlı, S.B. Smith, S.M. Smith, R. Socodato, Marco Spinazzi, K. Srinivasan, Philip Storey, María Fernanda Suárez, H.A. Tajmir-Riahi, Gavin S. Tan, Vin Tangpricha, Akihiko Tawara, P. Archana Teresa, Philip A. Thomas, Mehmet Tosun, Julio A. Urrets-Zavalía, Preejith P. Vachali, Carole Vaysse, Sabrina Viau, Claire M. Williams, Tien Y. Wong, Chen Xi, Ramazan Yağcı, Jia Yan, Baoru Yang, Ji Yong, Vicente Zanon-Moreno, Xiangjia Zhu, and S.R. Zwart

Published
2014

5. Quercetin and Glaucoma

Author

Kimitoshi Kohno, Akihiko Tawara, Hiroto Izumi, and Naoya Miyamoto

Subjects
chemistry.chemical_classification, Reactive oxygen species, genetic structures, business.industry, Glaucoma, Anatomy, Mitochondrion, Pharmacology, medicine.disease_cause, medicine.disease, Retinal ganglion, eye diseases, Endothelial stem cell, medicine.anatomical_structure, chemistry, medicine, Optic nerve, sense organs, Trabecular meshwork, business, Oxidative stress
Abstract

Glaucoma is a major cause of irreversible blindness and it has been predicted that 79.6 million people worldwide will suffer with glaucoma by 2020. Glaucoma is a progressive neuropathy characterized by the irreversible loss of retinal ganglion cells (RGCs), and it is a major cause of irreversible visual impairment, as damaged RGCs are incapable of repair or regeneration. Elevated intraocular pressure (IOP) due to a reduction in aqueous outflow is a major risk factor in the development of glaucoma and the progression of glaucomatous damage to the optic nerve. The trabecular meshwork (TM), which comprises endothelial-like cells, is the major location of aqueous humor outflow. These TM cells are critical for the maintenance of the aqueous humor outflow pathway. TM is known to be subjected to different types of stress such as oxidative stress. Oxidative stress is able to affect the cellularity of TM, and reported to trigger degeneration in the human TM and its endothelial cell components, subsequently leading to an increase in IOP and glaucoma. Increasing evidence indicates that reactive oxygen species (ROS) play a key role in the pathogenesis of glaucoma. Flavonoids such as quercetin (3,5,7,3′,4′-pentahydroxy flavone) can protect cells from oxidative stress. Quercetin is a natural and important dietary flavonoid compound that is widely distributed in fruit and vegetables. It has been shown that certain flavonoids can induce antioxidant responsive element-dependent gene expression through the activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2). This review supports the hypothesis that oxidative stress is an important step in the pathogenesis of glaucoma and quercetin might be a relevant target for both prevention and therapy.

Published
2014

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