Overexpression of survivin in primary ATL cells and sodium arsenite induces apoptosis by down-regulating survivin expression in ATL cell lines by Xiao-Fang.

Slides:



Advertisements
Similar presentations
Involvement of CD147 on multidrug resistance through the regulation of P-glycoprotein expression in K562/ADR leukemic cell line  Aoranit Somno, Songyot.
Advertisements

by Elena A. Federzoni, Peter J. M. Valk, Bruce E
MMP-2, MT1-MMP, and TIMP-2 are essential for the invasive capacity of human mesenchymal stem cells: differential regulation by inflammatory cytokines by.
Comparison of Caspase Activation and Subcellular Localization in HL-60 and K562 Cells Undergoing Etoposide-Induced Apoptosis by Luis M. Martins, Peter.
Antiangiogenic antithrombin down-regulates the expression of the proangiogenic heparan sulfate proteoglycan, perlecan, in endothelial cells by Weiqing.
by Yoko Otake, Sridharan Soundararajan, Tapas K. Sengupta, Ebenezer A
by Susan E. Shetzline, Ravikumar Rallapalli, Kelley J
2-Methoxyestradiol overcomes drug resistance in multiple myeloma cells
by Pascal Gelebart, Mona Anand, Hanan Armanious, Anthea C
Curcumin (diferuloylmethane) down-regulates the constitutive activation of nuclear factor–κB and IκBα kinase in human multiple myeloma cells, leading to.
The TCL1 oncoprotein inhibits activation-induced cell death by impairing PKCθ and ERK pathways by Gilles Despouy, Marjorie Joiner, Emilie Le Toriellec,
STAT3-mediated constitutive expression of SOCS-3 in cutaneous T-cell lymphoma by Christine Brender, Mette Nielsen, Keld Kaltoft, Gitte Mikkelsen, Qian.
Aurora Kinase A Is Upregulated in Cutaneous T-Cell Lymphoma and Represents a Potential Therapeutic Target  Daniel Humme, Ahmed Haider, Markus Möbs, Hiroshi.
Constitutively activated phosphatidylinositol-3 kinase (PI-3K) is involved in the defect of apoptosis in B-CLL: association with protein kinase Cδ by Ingo.
Yongping Shao, Kaitlyn Le, Hanyin Cheng, Andrew E. Aplin 
by Kumudha Balakrishnan, William G. Wierda, Michael J
Droxinostat, a Histone Deacetylase Inhibitor, Induces Apoptosis in Hepatocellular Carcinoma Cell Lines via Activation of the Mitochondrial Pathway and.
Overexpression of ornithine decarboxylase enhances endothelial proliferation by suppressing endostatin expression by Takahiro Nemoto, Hisae Hori, Masataka.
CD74 induces TAp63 expression leading to B-cell survival
Aurora kinase inhibitory VX-680 increases Bax/Bcl-2 ratio and induces apoptosis in Aurora-A-high acute myeloid leukemia by Xue-Fei Huang, Shao-Kai Luo,
Retinoic acid–induced cell cycle arrest of human myeloid cell lines is associated with sequential down-regulation of c-Myc and cyclin E and posttranscriptional.
Activation of ATF4 mediates unwanted Mcl-1 accumulation by proteasome inhibition by Jinsong Hu, Nana Dang, Eline Menu, Elke De Bryune, Dehui Xu, Ben Van.
by Christopher J. Ott, Nadja Kopp, Liat Bird, Ronald M
by Rong Chen, Michael J. Keating, Varsha Gandhi, and William Plunkett
PTF1α/p48 and cell proliferation
Nanomolar concentration of NSC606985, a camptothecin analog, induces leukemic-cell apoptosis through protein kinase Cδ–dependent mechanisms by Man-Gen.
Effects of Betulinic Acid Alone and in Combination with Irradiation in Human Melanoma Cells  Edgar Selzer, Emilio Pimentel, Volker Wacheck, Werner Schlegel,
Inhibition of glycogen synthase kinase-3 activity leads to epigenetic silencing of nuclear factor κB target genes and induction of apoptosis in chronic.
Cathepsin-B-dependent apoptosis triggered by antithymocyte globulins: a novel mechanism of T-cell depletion by Marie-Cécile Michallet, Frederic Saltel,
by Jun Yuan, David B. Lovejoy, and Des R. Richardson
Vascular endothelial growth factor stimulates protein kinase CβII expression in chronic lymphocytic leukemia cells by Simon T. Abrams, Benjamin R. B. Brown,
by Shrikanth P. Hegde, JingFeng Zhao, Richard A. Ashmun, and Linda H
Cell-surface CD74 initiates a signaling cascade leading to cell proliferation and survival by Diana Starlets, Yael Gore, Inbal Binsky, Michal Haran, Nurit.
by Eleanor J. Molloy, Amanda J. O'Neill, Julie J
The BH3-mimetic GX synergizes with bortezomib in mantle cell lymphoma by enhancing Noxa-mediated activation of Bak by Patricia Pérez-Galán, Gaël.
Small-molecule XIAP inhibitors derepress downstream effector caspases and induce apoptosis of acute myeloid leukemia cells by Bing Z. Carter, Marcela Gronda,
Fas ligand+ fallopian tube epithelium induces apoptosis in both Fas receptor+ T lymphocytes and endometrial cells  Sebastian E. Illanes, M.D., Kevin Maisey,
Indomethacin Sensitizes TRAIL-Resistant Melanoma Cells to TRAIL-Induced Apoptosis through ROS-Mediated Upregulation of Death Receptor 5 and Downregulation.
Stimulation of the B-cell receptor activates the JAK2/STAT3 signaling pathway in chronic lymphocytic leukemia cells by Uri Rozovski, Ji Yuan Wu, David.
Bone morphogenetic protein-2 induces apoptosis in human myeloma cells with modulation of STAT3 by Chiharu Kawamura, Masahiro Kizaki, Kenji Yamato, Hideo.
Synergistic Cytotoxicity of Sorafenib with Busulfan and Nucleoside Analogs in Human FMS-like Tyrosine Kinase 3 Internal Tandem Duplications–Positive Acute.
Soluble PD-1 ligands regulate T-cell function in Waldenstrom macroglobulinemia by Shahrzad Jalali, Tammy Price-Troska, Jonas Paludo, Jose Villasboas, Hyo-Jin.
Volume 136, Issue 4, Pages (April 2009)
Volume 6, Issue 2, Pages (August 2002)
Endoplasmic reticulum stress is a target for therapy in Waldenstrom macroglobulinemia by Xavier Leleu, Lian Xu, Xiaoying Jia, Antonio Sacco, Mena Farag,
Akio Horiguchi, Mototsugu Oya, Ken Marumo, Masaru Murai 
Volume 118, Issue 6, Pages (June 2000)
Anne T. Funding, Claus Johansen, Matthias Gaestel, Bo M
Apoptosis Induction by SAHA in Cutaneous T-Cell Lymphoma Cells Is Related to Downregulation of c-FLIP and Enhanced TRAIL Signaling  Nadya Al-Yacoub, Lothar.
Volume 11, Issue 6, Pages (June 2003)
Resistance of Human Melanoma Cells Against the Death Ligand TRAIL Is Reversed by Ultraviolet-B Radiation via Downregulation of FLIP  Elke Zeise, Michael.
PPARδ Is a Type 1 IFN Target Gene and Inhibits Apoptosis in T Cells
Collagen Synthesis Is Suppressed in Dermal Fibroblasts by the Human Antimicrobial Peptide LL-37  Hyun Jeong Park, Dae Ho Cho, Hee Jung Kim, Jun Young.
Expression and activation of caspase-3/CPP32 in CD34+ cord blood cells is linked to apoptosis after growth factor withdrawal  Li-Sheng Wang, Hong-Jun.
Volume 18, Issue 3, Pages (March 2010)
Thiocolchicoside inhibits TNF-dependent IκBα phosphorylation, IκBα degradation, p65 phosphorylation, and p65 nuclear translocation. Thiocolchicoside inhibits.
Knocking down Wnt3 increases the cells' response to trastuzumab and reduces cells' invasiveness. Knocking down Wnt3 increases the cells' response to trastuzumab.
Volume 3, Issue 5, Pages (May 2001)
Correlation of MAGE-A1 expression with PFS in patients treated with FRD and knockdown of MAGE-A in HMCLs. MAGE-A1 expression is correlated with resistance.
Ectopic expression of caveolin-1 in ZR75 human breast cancer cells downregulated survivin and decreased cell proliferation. Ectopic expression of caveolin-1.
Bcl-2 and bcl-xL Antisense Oligonucleotides Induce Apoptosis in Melanoma Cells of Different Clinical Stages  Robert A. Olie, Christoph Hafner, Renzo Küttel,
The Akt/Mcl-1 pathway plays a prominent role in mediating antiapoptotic signals downstream of the B-cell receptor in chronic lymphocytic leukemia B cells.
Lamellarin D induces cell death through a Fas-independent pathway.
Lamellarin D activates the intrinsic pathway of apoptosis.
A. A. Honokiol inhibits TNF-induced NF-κB activation, IκBα phosphorylation, and IκBα degradation. Honokiol inhibits TNF-induced activation of NF-κB. H1299.
by Dana S. Levy, Jason A. Kahana, and Rakesh Kumar
AS1411 alters subcellular distribution of PRMT5 in a time-dependent, dose-dependent, and nucleolin-dependent manner. AS1411 alters subcellular distribution.
Effect of bevacizumab on the proliferation of A2780 cells.
Expression and induction of HER2 and HPSE in 231BMBC cells.
Effect of SFN on the total activity and protein expression of HDACs in JB6 P+ cells. Effect of SFN on the total activity and protein expression of HDACs.
Presentation transcript:

Overexpression of survivin in primary ATL cells and sodium arsenite induces apoptosis by down-regulating survivin expression in ATL cell lines by Xiao-Fang Che, Chun-Lei Zheng, Satsuki Owatari, Masato Mutoh, Takenari Gotanda, Hei-Cheul Jeung, Tatsuhiko Furukawa, Ryuji Ikeda, Masatatsu Yamamoto, Misako Haraguchi, Naomichi Arima, and Shin-ichi Akiyama Blood Volume 107(12):4880-4887 June 15, 2006 ©2006 by American Society of Hematology

IAP family mRNA expression. IAP family mRNA expression. A quantitative RT-PCR analysis for survivin (A), cIAP1 (B), and XIAP (C) is shown in patients with acute, chronic, and smoldering ATL and in a healthy control (left), low PS and high PS (right). Each mRNA expression level was normalized on the basis of the GAPDH mRNA expression and expressed relative to the mRNA level in a healthy control. Boxes correspond to the interquartile range. Lines in the boxes represent median values. The vertical lines represent the 10th and 90th percentiles, and the circles represent the outliers. Differences were analyzed by Mann-Whitney's U test. Xiao-Fang Che et al. Blood 2006;107:4880-4887 ©2006 by American Society of Hematology

Protein expression of survivin in ATL Protein expression of survivin in ATL. Whole-cell lysates (50 μg protein) from patients with ATL were separated by 12.5% SDS-PAGE and then transferred to a PVDF membrane. Protein expression of survivin in ATL. Whole-cell lysates (50 μg protein) from patients with ATL were separated by 12.5% SDS-PAGE and then transferred to a PVDF membrane. The transferred proteins were reacted with antibody against survivin (A) as described in “Patients, materials, and methods.” *Concentrations of survivin protein and mRNA are expressed relative to the survivin protein and mRNA levels in control normal cells, which were assigned values of 1. (B) A comparison between the survivin mRNA level (y-axis) and the protein expression level (x-axis) in 17 patients with ATL. The survivin mRNA level correlated with the protein level (r = 0.516, P = .033). Xiao-Fang Che et al. Blood 2006;107:4880-4887 ©2006 by American Society of Hematology

The effects of sodium arsenite on the survivin expression in ATL cells. The effects of sodium arsenite on the survivin expression in ATL cells. (A) MT2, S1T, and Jurkat cells were incubated in the presence of 2 or 5 μM arsenic trioxide for 24, 48, or 72 hours. Whole-cell lysates (100 μg protein) were prepared and separated by 12.5% SDS-PAGE and transferred to a PVDF membrane. The transferred proteins were reacted with the antibody against survivin, Bcl-2, or PARP as described in “Patients, materials, and methods.” As an internal control, α-tubulin expression was detected. (B) The quantification of the survivin levels in MT2, S1T, and Jurkat cells. The relative density of the bands for survivin obtained by a densitometric analysis and α-tubulin was used to normalize the respective intensities. (C) S1T and Jurkat cells were treated with sodium arsenite at the indicated concentration and time. Total RNA was then subjected to RT-PCR using primers specific for the amplification of survivin. β-actin expression was examined as an internal control to ensure the RNA integrity and proper amplification. Xiao-Fang Che et al. Blood 2006;107:4880-4887 ©2006 by American Society of Hematology

Growth inhibition of MT2, S1T, and Jurkat cells by sodium arsenite. Growth inhibition of MT2, S1T, and Jurkat cells by sodium arsenite. Proliferation of MT2 (A), S1T (B), and Jurkat (C) cells in the absence or presence of the indicated concentrations of sodium arsenite was assessed by MTT assay. (D) The sodium arsenite toxicity in MT2, S1T, and Jurkat cells was determined by an MTT assay. The points represent the means of triplicate determinations, while the bars show SD. Xiao-Fang Che et al. Blood 2006;107:4880-4887 ©2006 by American Society of Hematology

Effects of sodium arsenite on the proportion of sub-G1 fraction of MT2, S1T, and Jurkat cells. Effects of sodium arsenite on the proportion of sub-G1 fraction of MT2, S1T, and Jurkat cells. MT2, S1T, and Jurkat cells were treated with 0, 1, 2, 5, or 10 μM sodium arsenite for 1, 2, or 3 days. The cells were then stained by propidium iodide (PI) and analyzed by flow cytometry. The proportion of sub-G1 fraction of MT2 (A) and S1T (B) was higher than that of Jurkat cells (C) under the indicated concentrations of sodium arsenite and the indicated time. Each column and bar represents the mean ± SD of 3 independent experiments. (D) The sub-G1 fraction of MT2, S1T, and Jurkat cells treated with sodium arsenite for 3 days was compared. Each column and bar represents the mean ± SD of 3 independent experiments. *P < .01. Xiao-Fang Che et al. Blood 2006;107:4880-4887 ©2006 by American Society of Hematology

The activities of caspase-3 in MT2 and S1T cells in the absence or presence of sodium arsenite. The activities of caspase-3 in MT2 and S1T cells in the absence or presence of sodium arsenite. The caspase-3 activity was measured in the cell lysates using the specific substrate Ac-DEVD-MCA. The data are expressed in arbitrary units. Each value represents the mean of 3 independent experiments. Bars indicate SD. *P < .01. Xiao-Fang Che et al. Blood 2006;107:4880-4887 ©2006 by American Society of Hematology

The effect of sodium arsenite on the levels of IκB-α, NF-κB, and survivin in nuclear and cytosolic fraction from MT2 and S1T cells. The effect of sodium arsenite on the levels of IκB-α, NF-κB, and survivin in nuclear and cytosolic fraction from MT2 and S1T cells. (A) MT2 cells were treated with sodium arsenite at the indicated concentrations; nuclear and cytosolic fractions were prepared at the indicated time. Nuclear protein (50 μg) was subjected to Western blotting using the antibody against p50, p65, or survivin. Cytoplasmic fraction (100 μg of protein) was subjected to Western blotting using the specific antibody against IκB-α or survivin. α-tubulin expression was used as a loading control. NE indicates nuclear extract; CE, cytoplasmic extract. *Nonspecific band. (B) p50 and p65 in the nucleus and cytoplasmic survivin in S1T cells treated with sodium arsenite in the indicated concentration, and time was measured by Western blot as in panel A. Xiao-Fang Che et al. Blood 2006;107:4880-4887 ©2006 by American Society of Hematology

Expression of MRP1 and the resistance to sodium arsenite in Jurkat cells. Expression of MRP1 and the resistance to sodium arsenite in Jurkat cells. (A) Crude membranes (100 μg protein) were prepared and separated by 7.5% SDS-PAGE and transferred to a PVDF membrane. The transferred proteins were reacted with an antibody against MRP1 as described in “Patients, materials, and methods.” KB/MRP membrane vesicles (10 μg) were used as a positive control. (B) Jurkat and S1T cells were incubated with the indicated concentrations of drugs for 72 hours, and cell viability was determined by the MTT assay. The points represent the means of triplicate determinations, and the bars show SD. Xiao-Fang Che et al. Blood 2006;107:4880-4887 ©2006 by American Society of Hematology