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17 results on '"Hideshima, Hiromasa"'

9. Akt Inhibitor Perifosine-Induced Cytotoxicity Is Associated with Significant Downregulation of Survivin in Human Multiple Myeloma (MM) Cells.

Author

Hideshima, Teru, primary, Yasui, Hiroshi, additional, Catley, Laurence, additional, Raje, Noopur, additional, Chauhan, Dharminder, additional, Ishitsuka, Kenji, additional, Podar, Klaus, additional, Mitsiades, Constantine, additional, Tai, Yu-Tzu, additional, Vallet, Sonia, additional, Kizitepe, Tanyel, additional, Ocio, Enrique, additional, Ikeda, Hiroshi, additional, Okawa, Yutaka, additional, Hideshima, Hiromasa, additional, Munshi, Nikhil C., additional, Richardson, Paul G., additional, and Anderson, Kenneth C., additional

Published
2006
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10. Honokiol overcomes conventional drug resistance in human multiple myeloma by induction of caspase-dependent and -independent apoptosis

Author

Ishitsuka, Kenji, primary, Hideshima, Teru, additional, Hamasaki, Makoto, additional, Raje, Noopur, additional, Kumar, Shaji, additional, Hideshima, Hiromasa, additional, Shiraishi, Norihiko, additional, Yasui, Hiroshi, additional, Roccaro, Aldo M., additional, Richardson, Paul, additional, Podar, Klaus, additional, Le Gouill, Steven, additional, Chauhan, Dharminder, additional, Tamura, Kazuo, additional, Arbiser, Jack, additional, and Anderson, Kenneth C., additional

Published
2005
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11. P38 MAPK Inhibition Enhances PS-341 (bortezomib)-Induced Cytotoxicity Against Multiple Myeloma Cells.

Author

Hideshima, Teru, primary, Podar, Klaus, additional, Chauhan, Dharminder, additional, Ishitsuka, Kenji, additional, Mitsiades, Constantine, additional, Tai, Yu-Tzu, additional, Hamasaki, Makoto, additional, Raje, Noopur, additional, Hideshima, Hiromasa, additional, Schreiner, George, additional, Nguyen, Aaron, additional, Navas, Tony, additional, Munshi, Nikhil C., additional, Richardson, Paul G., additional, Higgins, Linda S., additional, and Anderson, Kenneth C., additional

Published
2004
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12. Honokiol Overcomes Conventional Drug Resistance in Human Multiple Myeloma.

Author

Ishitsuka, Kenji, primary, Hideshima, Teru, additional, Hamasaki, Makoto, additional, Noopur, Raje, additional, Shaji, Kumar, additional, Hideshima, Hiromasa, additional, Shiraishi, Norihiko, additional, Richardson, Paul, additional, Munshi, Nikhil C., additional, Chauhan, Dharminder, additional, Arbiser, Jack, additional, and Anderson, Kenneth C., additional

Published
2004
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13. Targeting IKK Inhibits Multiple Myeloma (MM) Cell Growth in the Bone Marrow Microenvironment.

Author

Hideshima, Teru, primary, Tassone, Pierfrancesco, additional, Chauhan, Dharminder, additional, Ishitsuka, Kenji, additional, Mitsiades, Constantine, additional, Raje, Noopur, additional, Kumar, Shaji, additional, Hamasaki, Makoto, additional, Hideshima, Hiromasa, additional, Munshi, Nikhil C., additional, Richardson, Paul G., additional, Schenkein, David, additional, and Anderson, Kenneth C., additional

Published
2004
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14. Molecular Characterization of PS-341 (bortezomib) Resistance: Implications for Overcoming Resistance Using Lysophosphatidic Acid Acyltransferase (LPAAT)-β Inhibitors.

Author

Hideshima, Teru, primary, Chauhan, Dharminder, primary, Ishitsuka, Kenji, primary, Raje, Noopur, primary, Kumar, Shaji, primary, Podar, Klaus, primary, Mitsiades, Constantine, primary, Hideshima, Hiromasa, primary, Bonham, Lynn, primary, Munshi, Nikhil C., primary, Richardson, Paul G., primary, Singer, Jack W., primary, and Anderson, Kenneth C., primary

Published
2004
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15. Molecular characterization of PS-341 (bortezomib) resistance: implications for overcoming resistance using lysophosphatidic acid acyltransferase (LPAAT)-ßinhibitors.

Author

Hideshima, Teru, Chauhan, Dharminder, Ishitsuka, Kenji, Yasui, Hiroshi, Raje, Noopur, Kumar, Shaji, Podar, Klaus, Mitsiades, Constantine, Hideshima, Hiromasa, Bonham, Lynn, Munshi, Nikhil C, Richardson, Paul G, Singer, Jack W, and Anderson, Kenneth C

Subjects
APOPTOSIS, CELL death, MONOCLONAL gammopathies, ANTHRACYCLINES, LYSOPHOSPHOLIPIDS, ACYLTRANSFERASES
Abstract

PS-341 (bortezomib, Velcade™) is a promising novel agent for treatment of advanced multiple myeloma (MM); however, 65%of patients with relapsed refractory disease in a phase II study do not respond to PS-341. We have previously shown that lysophosphatidic acid acyltransferase (LPAAT)-ßinhibitor CT-32615 triggers caspase-dependent apoptosis, and can overcome resistance to conventional therapeutics (i.e., dexamethasone, doxorubicin, melphalan) in MM cells. In this study, we therefore determined whether CT-32615 could also overcome resistance to PS-341. We first characterized molecular mechanisms of resistance to PS-341 in DHL-4 cells. DHL-4 cells express low levels of caspase-3 and caspase-8; furthermore, no cleavage in caspase-8, caspase-9, caspase-3, poly ADP-ribose polymerase (PARP), or DNA fragmentation factor 45 was triggered by PS-341 treatment. We have previously shown that PS-341 treatment triggers phosphorylation of c-Jun NH2-terminal kinase (JNK), which subsequently induces caspase-dependent apoptosis; conversely, JNK inhibition blocks PS-341-induced apoptosis. We here show that phosphorylation of SEK-1, JNK, and c-Jun are not induced by PS-341 treatment, suggesting that PS-341 does not trigger a stress response in DHL-4 cells. Importantly, CT-32615 inhibits growth of DHL-4 cells in a time- and dose-dependent fashion: a transient G2/M cell cycle arrest induced by CT-32615 is mediated via downregulation of cdc25c and cdc2. CT-32615 triggered swelling and lysis of DHL-4 cells, without caspase/PARP cleavage or TUNEL-positivity, suggesting a necrotic response. Our studies therefore demonstrate that LPAAT-ßinhibitor CT-32615 triggers necrosis, even in PS-341-resistant DHL-4 cells, providing the framework for its evaluation to overcome clinical PS-341 resistance and improve patient outcome.Oncogene (2005) 24, 3121-3129. doi:10.1038/sj.onc.1208522 Published online 21 February 2005 [ABSTRACT FROM AUTHOR]

Published
2005
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16. A proto-oncogene BCL6is up-regulated in the bone marrow microenvironment in multiple myeloma cells

Author

Hideshima, Teru, Mitsiades, Constantine, Ikeda, Hiroshi, Chauhan, Dharminder, Raje, Noopur, Gorgun, Gullu, Hideshima, Hiromasa, Munshi, Nikhil C., Richardson, Paul G., Carrasco, Daniel R., and Anderson, Kenneth C.

Abstract

Constitutive B-cell lymphoma 6 (Bcl-6) expression was undetectable in multiple myeloma (MM) cell lines, except U266 cells. However, it was up-regulated by coculture with bone marrow (BM) stromal cell-culture supernatant (SCCS). Bcl-6 expression in patient MM cells in the BM was positive. Anti–interleukin-6 (IL-6)–neutralizing antibody significantly blocked SCCS-induced Bcl-6 in MM cells. Indeed, IL-6 strongly triggered Bcl-6 expression in MM cells, whereas Janus kinase inhibitor and STAT3 siRNA down-regulated Bcl-6. Tumor necrosis factor-α (TNF-α) also triggered Bcl-6, but independently of STAT3, whereas IκB kinaseβ inhibitor down-regulated TNF-α–induced Bcl-6, indicating that the canonical nuclear factor-κB pathway mediates TNF-α–induced Bcl-6 expression. Importantly, down-regulation of Bcl-6 by shRNA significantly inhibited MM cell growth in the presence of SCCS. Our results therefore suggest that Bcl-6 expression in MM cells is modulated, at least in part, via Janus kinase/STAT3 and canonical nuclear factor-κB pathways and that targeting Bcl-6, either directly or via these cascades, inhibits MM cell growth in the BM milieu.

Published
2010
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17. Zfat-deficient CD4⁺ CD8⁺ double-positive thymocytes are susceptible to apoptosis with deregulated activation of p38 and JNK.

Author

Ishikura S, Ogawa M, Doi K, Matsuzaki H, Iwaihara Y, Tanaka Y, Tsunoda T, Hideshima H, Okamura T, and Shirasawa S

Subjects
Animals, Apoptosis drug effects, Apoptosis genetics, Apoptosis physiology, Cell Differentiation drug effects, Cell Differentiation genetics, Cell Differentiation physiology, Flow Cytometry, Mice, Mice, Mutant Strains, Phosphorylation, Receptors, Antigen, T-Cell metabolism, Thymocytes drug effects, Transcription Factors genetics, CD4-Positive T-Lymphocytes cytology, CD4-Positive T-Lymphocytes metabolism, CD8-Positive T-Lymphocytes cytology, CD8-Positive T-Lymphocytes metabolism, JNK Mitogen-Activated Protein Kinases metabolism, Thymocytes cytology, Thymocytes metabolism, Transcription Factors deficiency, p38 Mitogen-Activated Protein Kinases metabolism
Abstract

Zfat, which is a nuclear protein harboring an AT-hook domain and 18-repeats of C2H2 zinc-finger motif, is highly expressed in immune-related tissues, including the thymus and spleen. T cell specific deletion of the Zfat gene by crossing Zfat(f/f) mice with LckCre mice yields a significant reduction in the number of CD4(+) CD8(+) double-positive (DP) thymocytes. However, physiological role for Zfat in T cell development in the thymus remains unknown. Here, we found that Zfat-deficient DP thymocytes in Zfat(f/f)-LckCre mice were susceptible to apoptosis both at an unstimulated state and in response to T cell receptor (TCR)-stimulation. The phosphorylation levels of p38 and JNK were elevated in Zfat-deficient thymocytes at an unstimulated state with an enhanced phosphorylation of ATF2 and with an over-expression of Gadd45α⋅ On the other hand, the activation of JNK in the Zfat-deficient thymocytes, but not p38, was strengthened and prolonged in response to TCR-stimulation. All these results demonstrate that Zfat critically participates in the development of DP thymocytes through regulating the activities of p38 and JNK., (© 2014 Wiley Periodicals, Inc.)

Published
2015
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