Search

Your search keyword '"Sauane, Moira"' showing total 155 results
Start Over Author "Sauane, Moira"
155 results on '"Sauane, Moira"'

3. Interleukin 24: Signal Transduction Pathways

Author

Smith, Simira, primary, Lopez, Sual, additional, Kim, Anastassiya, additional, Kasteri, Justina, additional, Olumuyide, Ezekiel, additional, Punu, Kristian, additional, de la Parra, Columba, additional, and Sauane, Moira, additional

Published
2023
Full Text
View/download PDF

11. Analysis of Adult Neural Retina Extracellular Vesicle Release, RNA Transport and Proteomic Cargo

Author

Mighty, Jason, primary, Zhou, Jing, additional, Benito-Martin, Alberto, additional, Sauma, Sami, additional, Hanna, Samer, additional, Onwumere, Onyekwere, additional, Shi, Cui, additional, Muntzel, Martin, additional, Sauane, Moira, additional, Young, Michael, additional, Molina, Henrik, additional, Cox, Dianne, additional, and Redenti, Stephen, additional

Published
2020
Full Text
View/download PDF

12. The development of MDA-7/IL-24 as a cancer therapeutic

Author

Dent, Paul, Yacoub, Adly, Hamed, Hossein A., Park, Margaret A., Dash, Rupesh, Bhutia, Sujit K., Sarkar, Devanand, Wang, Xiang-Yang, Gupta, Pankaj, Emdad, Luni, Lebedeva, Irina V., Sauane, Moira, Su, Zhao-zhong, Rahmani, Mohamed, Broaddus, William C., Young, Harold F., Lesniak, Maciej S., Grant, Steven, Curiel, David T., and Fisher, Paul B.

Published
2010
Full Text
View/download PDF

17. A Self-degradable Curcumin Polymer with Anti-cancer Activity

Author

O’Connor, Naphtali A., Einbond, Linda S., Redenti, Stephen, Sauane, Moira, and Jitianu, Andrei

Subjects
Article
Abstract

Curcumin is a widely researched and utilized natural product used for a variety of ailments including as a gastrointestinal aide and an anticancer agent. Curcumin however suffers from poor bioavailability. A strategy to circumvent poor bioavailability is to administer with an adjuvant or by synthetic modification. Herein we demonstrate the incorporation of curcumin into a self-degradable polymer by condensation with N,N′-di-Boc-L-cystine. The polymer is made self-degradable upon deprotection of the cystine amines. Degradation is confirmed by thermogravimetric analysis and differential scanning calorimetry. Curcumin retains its anti-cancer activity within the polymer showing activity against HT29 human colon cancer cells and DU-145 prostate cancer cells. The self-degrading polymer showed enhanced activity against HT29 cells compared to that of curcumin.

Published
2018

21. Translation Control by p53

Author

Kasteri, Justina, primary, Das, Dibash, additional, Zhong, Xuelin, additional, Persaud, Leah, additional, Francis, Ashleigh, additional, Muharam, Hilal, additional, and Sauane, Moira, additional

Published
2018
Full Text
View/download PDF

30. Signal transduction pathways in the mitogenic response to PGF 2 alfa LIF and related cytokines in Swiss 3T3 cells, including cyclins Ds and CDKs expression by diverse signalling pathways

Author

Sauane, Moira and Jiménez de Asúa, Luis

Subjects
ONCOSTATINA M (OSM), MITOGEN-ACTIVATED PROTEIN KINASE (MAPK), CITOQUINAS DE TIPO IL-6, FACTOR INHIBIDOR DE LA LEUCEMIA (LIF), PROTEIN KINASE A (PKA), CALCIUM, PROTEINAS QUINASAS DEPENDIENTES DE AMPC (PTK), MOLECULAS REGULATORIAS DEL CICLO CELULAR, SIGNALLING MECHANISMS, TGFBETA1, SWISS 3T3 CELLS, G1 PHASE, CYCLIN-D, MECANISMOS DE TRANSDUCCION DE SEÑAES, AMPC, GROWTH FACTORS, CILIARY NEUROTROPHIC FACTOR (CNTF), CELL CYCLE, PROSTAGLANDIN 2ALPHA (PGF 2ALPHA), PROTEINAS QUINASAS DE TIROSINAS (PKT), QUINASAS DEPENDIENTES DE CICLINAS (CDK), CALCIO, CYCLIN-DEPENDANT KINASE (CDK), CICLINAS D, PROTEIN TYROSINE KINASE (PKT), FACTORES DE CRECIMIENTO, PGF2ALFA, PROTEINA QUINASA C (PKC), LEUKAEMIA INHIBITORY FACTOR (LIF), SIGNAL TRANSDUCERS AND ACTIVATORS OF TRANSCRIPTION (STATS), FASE G1, ONCOSTATIN M (OSM), INTERLEUKIN-6 (IL-6), CELULAS DE RATON SWISS 3T3, TRANSFORMING GROWTH FACTOR BETA1 (TGFBETA1), TRANSDUCTORES DE SEÑALES Y FACTORES DE TRANSCRIPCION (STATS)
Abstract

Mammalian cell division, is a highly complex process, regulated and coordinated bymechanisms that are conserved through most species. The physiological control of eucarioticcell proliferation initiation is external, and it is excerted by humoral factors, made by the same orother cells, under certain requirements of the organism. Progression through the differentphases of the cell cycle, is governed by a regulatory machinery conserved through mostspecies, that not only coordinates the various events that made up the cell cycle, but alsoconnects the cell cycle with extracellular signals, that regulates cell proliferation. Beginning witha given mitogenic stimulus acting through a specific receptor in a target cell, signallingmechanisms cascades are generated in the membrane and in the citosol of that cell. Theseearly events, act on the cell cycle machinery, finally leading to cell division. The expression ofproteins that regulate the cell cycle is in part induced by mitogen-stimulated signallingmechanisms. The passage from G0 to S phase, depends on the activity of cyclin-dependent kinases (CDKs). These kinases are CDK4 and CDK6, and they are activated when they form complexes withcyclins D (D1, D2 and D3), induced in the G1 phase. Cyclins D are considered as "sensors" ofthe extracellular medium, since their induction is triggered by mitogenic stimuli. The activatedcomplexes cyclin D-CDK4 and cyclin D-CDKG catalyse the phosphorilation of the Rb protein. In Swiss 3T3 cells, PGF2α is capable of inducing DNA synthesis, by means of multiple signallingmechanisms, in the absence of other factors. However its mitogenic effect is potentiated by TGFβ1 addition. We have shown that PGF2α triggers cyclin D1 mRNA/protein expression prior tocellular entry into the S phase, but fails to raise CDK4 or cyclin D3 levels, while 1-oleoyl-2acetyllglycerol (OAG), a protein kinase C (PKC) and tyrosine kinase (TK) activator, induces onlycyclin D1 expression with no mitogenic response. In contrast, in PKC-depleted or -inhibited cells, PGF2α, but not OAG, increases cyclin D1 expression with no mitogenic response. Finally, OAG,in the presence of orthovanadate (Na3VO4)or TGFβ1, induces DNA synthesis. Thus, it appearsthat PGF2α triggers cyclin D1 expression via two independent signalling events that complementwith TGFβ1-triggered events to induce DNA synthesis. TGFβ1 cannot trigger cyclin D1expression, but, stabilise cyclin D1 mRNA, after PGF2α-triggered its expression. Leukaemia inhibitory factor (LIF) was originally described on the basis of its ability to stimulatethe differentiation of murine M1 leukemic cells into granulocytes and macrophages. In Swiss 3T3cells, both LIF and prostaglandin F2α (PGF2α) trigger initiation of DNA synthesis and cellproliferation. LIF appears to exert its action through signals and processes markedly differentfrom those elicited by PGF2α. While pre-treatment the cell culture with either GF 109203 (bysoindolmalemide), a specific PKC inhibitor, or 12-tetradecanoyl-13-phorbolacetate, whichcauses PKC down modulation, or lovastatin, known to block mevalonic acid synthesis andprotein isoprenylation, totally impairs PGF2α mitogenic action. None of these treatments inhibited LIF-induced DNA replication. Agents capable of rising intracellular cAMP, enhanced both LIFand PGF2α ability to cause cellular entry into the S phase. However, H89 and PKI, both PKAinhibitors, prevented cAMP-mediated potentiation, but did not affect LIF induction of cellularentry into S phase. PD98059, a MEK (MAPKK)inhibitor, prevents PGF2α-mitogenic responsebut does not block LIF-induced initiation of DNA synthesis. Immunofluorescence studiesrevealed that LIF and PGF2α responses exhibit marked differences in STAT cytoplasmic-nucleartranslocation. After 15 to 30 min, LIF causes STAT1 but not STAT3 or STAT5 translocation. Incontrast, PGF2α failed to induce translocation of any of those transcriptional factors. Thus, it appears that LIF triggers mitogenic action through independent signalling events suchas those involving PKC, PKA, MEK, p38MAPK and protein isoprenilation. In addition, its mitogeniceffect is markedly potentiated by PKC, PKA, and probably PTK mediated signallingmechanisms. Western blot analyses of cyclin D1, D2 and D3 expression (implicated in most mitogen actions),revealed that PGF2α, after 7-9 h, caused an increase in cyclin D1 protein levels, and a laterincrease in cyclin D2 levels. In contrast, LIF failed to increase either cyclin D1, D2, D3, CDK4 or CDK6 protein levels. Finally, oncostatin M(OSM), a cytokine closely related to LIF, exerts its action through signalsand processes markedly similar to those elicited by LIF. This conclusion is based in the followingfacts: both cytokines causes STAT1 tranlocation; the effect of Prostaglandin E1 and insulin,when added separately or in combination, enhances the effect of either LIF or OSM; PGF2αenhances the effect of LIF or OSM on DNA synthesis, both at subsaturant or saturantconcentration. Moreover, LIF and OSM added together at subsaturating concentrations had anadditive effect on DNA synthesis. LIF and OSM added together at saturating concentration hadan similar effect to that of these same cytokines when added separately. Interleukin -6 and CNTF, fail to cause either cyclin D expression or mitogenic response. The results obtained suggest that the PGF2α-stimulated mitogenesis would occur through cyclin D1 expression, mediated by DAG/PKC and TK dependent mechanisms, while calciumdependent mechanisms would be involved in other processes. Finally, the LlF stimulatedmitogenesis is not depend on signalling mechanisms such as those that act through PKC, PKA, MEK, p38MAPK and isoprenilated proteins, and also independently of the expression of cyclins D, CDK4 and CDK6. Fil: Sauane, Moira. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.

Published
2000

31. Breast Cancer Cell Selective Apoptosis Induced by the Novel Activity of an IL-10 Related Cytokine

Author

COLUMBIA UNIV NEW YORK, Sauane, Moira, COLUMBIA UNIV NEW YORK, and Sauane, Moira

Abstract

Preliminary data document that signaling events loading to Ad.mda-7-induced transformed-cell specific apoptosis are tyrosine kinase-independent. These results suggest that mda-7/IL-24 cancer cell-specific activity could occur through mechanisms independent of binding to its currently recognized cognate receptors and might even occur independent of receptor function. An adenovirus vector expressing a non-secreted version of MDA-7/IL-24 protein was generated via deletion of its signal peptide. This non-secreted protein was as effective as wild-type secreted MDA-7/IL-24 in inducing apoptosis in cancer cell lines, and displayed transformed cell specificity and localization of MDA-7/IL-24 in the Golgi/ER compartments. Based on localization as well as signal transduction pathway activation, MDA-7/IL-24 protein appears to induce ER stress that in turn induces proapoptotic events. A new reagent was generated i.e. a bacterially expressed and purified GST-MDA-7 fusion protein. We describe the properties and characteristics of this protein in this report. Treatment of breast cancer cell lines with GST-MDA-7 sensitizes both wild-type and mutant p53 expressing tumor cells to growth inhibitory and antisurvival effects of ionizing radiation. Our results indicate that mda-7/IL-24-mediated apoptosis can be triggered efficiently in the absence of protein secretion and is likely mediated by ER stress.

Published
2005

32. MDA-7/IL-24 as a cancer therapeutic: from bench to bedside

Author

Dent, Paul, primary, Yacoub, Adly, additional, Hamed, Hossein A., additional, Park, Margaret A., additional, Dash, Rupesh, additional, Bhutia, Sujit K., additional, Sarkar, Devanand, additional, Gupta, Pankaj, additional, Emdad, Luni, additional, Lebedeva, Irina V., additional, Sauane, Moira, additional, Su, Zhao-Zhong, additional, Rahmani, Mohamed, additional, Broaddus, William C., additional, Young, Harold F., additional, Lesniak, Maciej, additional, Grant, Steven, additional, Curiel, David T., additional, and Fisher, Paul B., additional

Published
2010
Full Text
View/download PDF

34. Historical perspective and recent insights into our understanding of the molecular and biochemical basis of the antitumor properties of mda-7/IL-24

Author

Emdad, Luni, primary, Lebedeva, Irina V., additional, Su, Zhao-zhong, additional, Gupta, Pankaj, additional, Sauane, Moira, additional, Dash, Rupesh, additional, Grant, Steven, additional, Dent, Paul, additional, Curiel, David T., additional, Sarkar, Devanand, additional, and Fisher, Paul B., additional

Published
2009
Full Text
View/download PDF

35. Caspase-, cathepsin-, and PERK-dependent regulation of MDA-7/IL-24-induced cell killing in primary human glioma cells

Author

Yacoub, Adly, primary, Park, Margaret A., additional, Gupta, Pankaj, additional, Rahmani, Mohammed, additional, Zhang, Guo, additional, Hamed, Hossein, additional, Hanna, David, additional, Sarkar, Devanand, additional, Lebedeva, Irina V., additional, Emdad, Luni, additional, Sauane, Moira, additional, Vozhilla, Nicollaq, additional, Spiegel, Sarah, additional, Koumenis, Costas, additional, Graf, Martin, additional, Curiel, David T., additional, Grant, Steven, additional, Fisher, Paul B., additional, and Dent, Paul, additional

Published
2008
Full Text
View/download PDF

36. mda-7/IL-24, novel anticancer cytokine: Focus on bystander antitumor, radiosensitization and antiangiogenic properties and overview of the phase I clinical experience (Review)

Author

Fisher, Paul, primary, Nemunaitis, John, additional, Senzer, Neil, additional, Dent, Paul, additional, Grant, Steven, additional, Yacoub, Adly, additional, Curiel, David, additional, Dmitriev, Igor, additional, Mahasreshti, Parameshwar, additional, De Pass, Anthony, additional, Inoue, Satoshi, additional, Chada, Sunil, additional, Li, Rong, additional, Ramesh, Rajagopal, additional, Boukerche, Habib, additional, Chatman, Lejuan, additional, Park, Eun, additional, Wang, Dongning, additional, Vozhilla, Nicollaq, additional, Lee, Seok-Geun, additional, Barral, Paola, additional, Xiao, Ruoyu, additional, Taher, Mohiuddin, additional, Liu, Shi-Jian, additional, Sauane, Moira, additional, Sarkar, Devanand, additional, Staudt, Michelle, additional, Gupta, Pankaj, additional, Su, Zao-Zhong, additional, Emdad, Luni, additional, and Lebedeva, Irina, additional

Published
2007
Full Text
View/download PDF

40. Leukemia Inhibitory Factor Induces DNA Synthesis in Swiss Mouse 3T3 Cells Independently of Cyclin D1 Expression through a Mechanism Involving MEK/ERK1/2 Activation

Author

Dekanty, Andres, primary, Sauane, Moira, additional, Cadenas, Belen, additional, Coluccio, Federico, additional, Barrio, Marcela, additional, Casala, Jorgelina, additional, Paciencia, Mercedes, additional, Rogers, Florencia, additional, Coso, Omar A., additional, Piwien-Pilipuk, Graciela, additional, Rudland, Philip S., additional, and de Asúa, Luis Jiménez, additional

Published
2006
Full Text
View/download PDF

41. mda-7/IL-24: Exploiting Cancer's Achilles' Heel

Author

Lebedeva, Irina V., primary, Sauane, Moira, additional, Gopalkrishnan, Rahul V., additional, Sarkar, Devanand, additional, Su, Zhao-zhong, additional, Gupta, Pankaj, additional, Nemunaitis, John, additional, Cunningham, Casey, additional, Yacoub, Adly, additional, Dent, Paul, additional, and Fisher, Paul B., additional

Published
2005
Full Text
View/download PDF

44. Methods for Analysing mRNA Expression

Author

Lorkowski, Stefan, primary, Cullen, Paul, additional, Horstmann, Sebastian, additional, Hess, Beate, additional, Langer, Claus, additional, Seedorf, Udo, additional, Gopalkrishnan, Rahul V., additional, Sarkar, Devanand, additional, Kang, Dong‐Chul, additional, Sivo, Frank, additional, Lebedeva, Irina V., additional, Leszczyniecka, Magdalena, additional, Sauane, Moira, additional, Goldstein, Neil I., additional, Fisher, Paul B., additional, Su, Zao‐Zhong, additional, Gerdemann, Carsten, additional, Sherwood, Anne, additional, Sarkar, Gobinda, additional, Zhang, Kunbo, additional, Bolander, Mark E., additional, Luo, Jian‐Hua, additional, Yu, Yan Ping, additional, Stolle, Katrin, additional, Wang, Zhou, additional, Brown, Donald D., additional, Wang, Yuxun, additional, Sytkowski, Arthur J., additional, Volsky, David J., additional, Jiang, Hongping, additional, Bowler, Lucas D., additional, Bouchardon, Annabelle, additional, Dehay, Colette, additional, Lavery, Daniel J., additional, Lackner, Karl J., additional, Roeder, Thomas, additional, Bruchhaus, Iris, additional, Kornmann, Benoît, additional, Rifat, Daniele, additional, Preitner, Nicolas, additional, Schibler, Ueli, additional, Bustin, Stephen A., additional, Theilgaard‐Mönch, Kim, additional, Rasmussen, Thomas, additional, Schnoor, Michael, additional, Kato, Kikuya, additional, Bachem, Christian W. B., additional, del Carmen, Asun Fernandes, additional, Visser, Richard G. F., additional, Hinojos, Cruz A., additional, Doris, Peter A., additional, Shmelkov, Sergey V., additional, Belyavsky, Alexander V., additional, Starkey, Michael P., additional, Mahadeva, Harin, additional, Bahn, Sabine, additional, Uematsu, Chihiro, additional, Miura, Fumihito, additional, Kambara, Hideki, additional, Nishida, Junko, additional, Okano, Kazunori, additional, Ito, Takashi, additional, Sakaki, Yoshiyuki, additional, Matz, Mikhail V., additional, and Watanabe, Sachihiko, additional

Published
2002
Full Text
View/download PDF

49. Ceramide plays a prominent role in MDA-7/IL-24-induced cancer-specific apoptosis.

Author

SAUANE, MOIRA, SU, ZAO-ZHONG, DASH, RUPESH, LIU, XIANG, NORRIS, JAMES S., SARKAR, DEVANAND, LEE, SEOK-GEUN, ALLEGOOD, JEREMY C., DENT, PAUL, SPIEGEL, SARAH, and FISHER, PAUL B.

Subjects
*MELANOMA, *INTERLEUKINS, *APOPTOSIS, *CANCER cells, *CERAMIDES, *CELL death
Abstract

Melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24) uniquely displays broad cancer-specific apoptosis-inducing activity through induction of endoplasmic reticulum (ER) stress. We hypothesize that ceramide, a promoter of apoptosis, might contribute to mda-7/IL-24 induction of apoptosis. Ad.mda-7-infected tumor cells, but not normal cells, showed increased ceramide accumulation. Infection with Ad.mda-7 induced a marked increase in various ceramides (C16, C24, C24:1) selectively in prostate cancer cells. Inhibiting the enzyme serine palmitoyltransferase (SPT) using the potent SPT inhibitor myriocin (ISP1), impaired mda-7/IL-24-induced apoptosis and ceramide production, suggesting that ceramide formation caused by Ad.mda-7 occurs through de novo synthesis of ceramide and that ceramide is required for mda-7/IL-24-induced cell death. Fumonisin B1 (FB1) elevated ceramide formation as well as apoptosis induced by Ad.mda-7, suggesting that ceramide formation may also occur through the salvage pathway. Additionally, Ad.mda-7 infection enhanced expression of acid sphingomyelinase (ASMase) with a concomitant increase in ASMase activity and decreased sphingomyelin in cancer cells. ASMase silencing by RNA interference inhibited the decreased cell viability and ceramide formation after Ad.mda-7 infection. Ad.mda-7 activated protein phosphatase 2A (PP2A) and promoted dephosphorylation of the anti-apoptotic molecule BCL-2, a downstream ceramide-mediated pathway of mda-7/IL-24 action. Pretreatment of cells with FB1 or ISP-1 abolished the induction of ER stress markers (BiP/GRP78, GADD153 and pospho-eIF2α) triggered by Ad.mda-7 infection indicating that ceramide mediates ER stress induction by Ad.mda-7. Additionally, recombinant MDA-7/IL-24 protein induced cancer-specific production of ceramide. These studies define ceramide as a key mediator of an ER stress pathway that may underlie mda-7/IL-24 induction of cancer-specific killing. J. Cell. Physiol. 222: 546–555, 2010. © 2009 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Published
2010
Full Text
View/download PDF

50. Leukemia Inhibitory Factor Induces DNA Synthesis in Swiss Mouse 3T3 Cells Independently of Cyclin D1 Expression through a Mechanism Involving MEK/ERK1/2 Activation.

Author

Dekanty, Andres, Sauane, Moira, Cadenas, Belen, Coluccio, Federico, Barrio, Marcela, Casala, Jorgelina, Paciencia, Mercedes, Rogers, Florencia, Coso, Omar A., Piwien-Pilipuk, Graciela, Rudland, Philip S., and Jiménez De Asúa, Luis

Subjects
*LEUKEMIA inhibitory factor, *DNA synthesis, *NEUROTROPHINS, *NEURON development, *INTERLEUKIN-6, *PROSTAGLANDINS, *RETINOBLASTOMA, *MESSENGER RNA
Abstract

Leukemia inhibitory factor (LIF) and oncostatin M (OSM) induce DNA synthesis in Swiss 3T3 cells through common signaling mechanism(s), whereas other related cytokines such as interleukin-6 and ciliary neurotrophic factor do not cause this response. Induction of DNA replication by LIF or prostaglandin F2α (PGF2α) occurs, in part, through different signaling events. LIF and OSM specifically trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF2α fails to do so. However, LIF and PGF2α can trigger increases in ERK1/2 activity, which are required for their mitogenic responses because U0126, a MEK1/2 inhibitor, prevents both ERK1/2 activation and induction of DNA synthesis by LIF or PGF2α treatment. PGF2α induces cyclin D expression and full phosphorylation of retinoblastoma protein. In contrast, LIF fails to promote increases in cyclin D mRNA/protein levels; consequently, LIF induces DNA synthesis without promoting full phosphorylation of retinoblastoma protein (Rb). However, both LIF and PGF2α increase cyclin E expression. Furthermore, LIF mitogenic action does not involve protein kinase C (PKC) activation, because a PKC inhibitor does not block this effect. In contrast, PKC activity is required for PGF2α mitogenic action. More importantly, the synergistic effect between LIF and PGF2α to promote S phase entry is independent of PKC activation. These results show fundamental differences between LIF- and PGF2α-dependent mechanism(s) that induce cellular entry into S phase. These findings are critical in understanding how LIF and other related cytokine-regulated events participate in normal cell cycle control and may also provide clues to unravel crucial processes underlying cancerous cell division. [ABSTRACT FROM AUTHOR]

Published
2006
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results