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  1. Article ; Online: Tobacco specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone suppresses a newly identified anti-tumor IGFBP-3/IGFBP-3R system in lung cancer cells.

    Harada, Aki / Jogie-Brahim, Sherryline / Oh, Youngman

    Lung cancer (Amsterdam, Netherlands)

    2013  Volume 80, Issue 3, Page(s) 270–277

    Abstract: IGFBP-3 is a tumor suppressor whose expression is frequently suppressed in lung cancer. NNK, the most potent tobacco carcinogen, enhanced cell proliferation of BEAS-2B normal lung epithelial cells and concomitantly suppressed IGFBP-3 expression through ... ...

    Abstract IGFBP-3 is a tumor suppressor whose expression is frequently suppressed in lung cancer. NNK, the most potent tobacco carcinogen, enhanced cell proliferation of BEAS-2B normal lung epithelial cells and concomitantly suppressed IGFBP-3 expression through DNA methylation. Decreased IGFBP-3 expression and elevated levels of phospho-Akt, phospho-p65-NF-κB, and cyclin D1 were detected in tobacco carcinogen-induced tumorigenic derivatives of BEAS-2B. Overexpression of IGFBP-3 in NNKA, one of the derivatives, suppressed NF-κB activity and induced apoptosis, which was hindered by knocking-down of endogenous IGFBP-3R, an IGFBP-3 specific receptor. These results suggest that NNK inhibits IGFBP-3 expression to abrogate anti-tumor actions of the IGFBP-3/IGFBP-3R system in smoking-induced lung cancer.
    MeSH term(s) Carcinogens/pharmacology ; Carcinogens/toxicity ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Insulin-Like Growth Factor Binding Protein 3/genetics ; Insulin-Like Growth Factor Binding Protein 3/metabolism ; Lung Neoplasms/etiology ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Nitrosamines/pharmacology ; Nitrosamines/toxicity ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Smoking/adverse effects ; Nicotiana/toxicity
    Chemical Substances Carcinogens ; IGFBP-3R protein, human ; Insulin-Like Growth Factor Binding Protein 3 ; Nitrosamines ; Receptors, Cell Surface ; 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (7S395EDO61)
    Language English
    Publishing date 2013-03-14
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 632771-0
    ISSN 1872-8332 ; 0169-5002
    ISSN (online) 1872-8332
    ISSN 0169-5002
    DOI 10.1016/j.lungcan.2013.02.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2135: Show issues Location:
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  2. Article ; Online: Unraveling insulin-like growth factor binding protein-3 actions in human disease.

    Jogie-Brahim, Sherryline / Feldman, David / Oh, Youngman

    Endocrine reviews

    2009  Volume 30, Issue 5, Page(s) 417–437

    Abstract: The IGF system plays critical roles in somatic growth in an endocrine fashion (somatomedin hypothesis) as well as proliferation and differentiation of normal and malignant cells in a paracrine/autocrine fashion. IGFBP-3 is known to modulate the actions ... ...

    Abstract The IGF system plays critical roles in somatic growth in an endocrine fashion (somatomedin hypothesis) as well as proliferation and differentiation of normal and malignant cells in a paracrine/autocrine fashion. IGFBP-3 is known to modulate the actions of IGFs in circulation as well as the immediate extracellular environment. Interestingly, apart from the ability to inhibit or enhance IGF actions, IGFBP-3 also exhibits very clear, distinct biological effects independent of the IGF/IGF-I receptor axis. Over the past decade it has become widely appreciated that IGF/IGF-IR-independent actions of IGFBP-3 (antiproliferative and proapoptotic effects) contribute to improving the pathophysiology of a variety of human diseases, such as cancer, diabetes, and malnutrition. Recent studies have implicated interaction of IGFBP-3 with a variety of proteins or signaling cascades critical to cell cycle control and apoptosis; however, the actual mechanism of IGFBP-3 action is still unclear. This review reinforces the concept in support of the IGF/IGF-IR axis-independent actions of IGFBP-3 and delineates potential underlying mechanisms involved and subsequent biological significance, focusing in particular on functional binding partners and the clinical significance of IGFBP-3 in the assessment of cancer risk.
    MeSH term(s) Active Transport, Cell Nucleus ; Animals ; Cell Differentiation ; Cell Nucleus/metabolism ; Cell Proliferation ; Conserved Sequence ; Gene Expression ; Humans ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor Binding Proteins/chemistry ; Insulin-Like Growth Factor Binding Proteins/genetics ; Insulin-Like Growth Factor Binding Proteins/physiology ; Neoplasms/epidemiology ; Polymorphism, Genetic ; Protein Binding ; Receptor, IGF Type 1/metabolism ; Receptors, Cell Surface ; Risk Factors ; Somatomedins/metabolism
    Chemical Substances IGFBP3 protein, human ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor Binding Proteins ; Receptors, Cell Surface ; Somatomedins ; Receptor, IGF Type 1 (EC 2.7.10.1)
    Language English
    Publishing date 2009-05-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 603096-8
    ISSN 1945-7189 ; 0163-769X
    ISSN (online) 1945-7189
    ISSN 0163-769X
    DOI 10.1210/er.2008-0028
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1562: Show issues Location:
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  3. Article ; Online: Insulin-like growth factor-binding protein-3 suppresses tumor growth via activation of caspase-dependent apoptosis and cross-talk with NF-κB signaling.

    Han, Jinfeng / Jogie-Brahim, Sherryline / Harada, Aki / Oh, Youngman

    Cancer letters

    2011  Volume 307, Issue 2, Page(s) 200–210

    Abstract: Nuclear factor-kappaB (NF-κB) is constitutively activated in a variety of human cancers including prostate cancer and involved in tumorigenesis, tumor progression and chemo-resistance. Insulin-like growth factor-binding protein-3 (IGFBP-3) is a potent ... ...

    Abstract Nuclear factor-kappaB (NF-κB) is constitutively activated in a variety of human cancers including prostate cancer and involved in tumorigenesis, tumor progression and chemo-resistance. Insulin-like growth factor-binding protein-3 (IGFBP-3) is a potent tumor suppressor and is significantly suppressed in a variety of cancers. Diverse biological effects of IGFBP-3 have been reported to be both dependent and independent of the IGF/IGF-I receptor (IGF-IR) axis. The precise underlying mechanisms of IGF/IGF-IR-independent, antiproliferative actions of IGFBP-3 are yet to be elucidated. We found an inverse correlation between NF-κB activity and IGFBP-3 expression during prostate cancer progression using an in vitro prostate cancer progression model. Restoration of IGFBP-3 resulted in significant inhibition of constitutively elevated NF-κB activity in prostate cancer cells. IGFBP-3 further inhibited the expression of NF-κB-regulated angiogenic factors such as VEGF and IL-8, and cell adhesion molecules, ICAM-1 and VCAM-1. This inhibitory action of IGFBP-3 was IGF/IGF-IR-independent since IGFBP-3 mutant devoid of IGF binding affinity had a similar inhibitory effect. We identified that IGFBP-3 degrades the key NF-κB regulatory molecules-IκBα and p65-NF-κB proteins through activation of caspase-8 and -3/-7, thereby inhibiting elevated NF-κB activity in prostate cancer. Finally intratumoral administration of IGFBP-3 resulted in significant tumor suppression as well as sensitization of antitumor effect of doxorubicin. Our findings indicate that IGFBP-3 exerts antitumor effects via IGF-independent mechanisms which involve activation of caspase-dependent apoptosis and cross-talk with NF-κB signaling. The use of IGFBP-3 as a cancer therapeutic with this distinctive suppression mechanism may offer alternate means to treat chemotherapy resistant tumors.
    MeSH term(s) Animals ; Apoptosis ; Base Sequence ; Blotting, Western ; Caspases/metabolism ; Cell Division/physiology ; Cell Line, Tumor ; DNA Primers ; Enzyme Activation ; Humans ; Immunohistochemistry ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor Binding Proteins/physiology ; Male ; Mice ; NF-kappa B/metabolism ; Polymerase Chain Reaction ; Prostatic Neoplasms/pathology ; RNA Processing, Post-Transcriptional ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction
    Chemical Substances DNA Primers ; IGFBP3 protein, human ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor Binding Proteins ; NF-kappa B ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2011-08-28
    Publishing country Ireland
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2011.04.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Potential of proteomics towards the investigation of the IGF-independent actions of IGFBP-3.

    Jogie-Brahim, Sherryline / Min, Hae-Ki / Oh, Youngman

    Expert review of proteomics

    2005  Volume 2, Issue 1, Page(s) 71–86

    Abstract: Early investigations into the insulin-like growth factor (IGF)-independent actions of insulin-like growth factor-binding protein (IGFBP)-3 have implicated a large array of signaling proteins with links to cell cycle control and apoptosis. However, the ... ...

    Abstract Early investigations into the insulin-like growth factor (IGF)-independent actions of insulin-like growth factor-binding protein (IGFBP)-3 have implicated a large array of signaling proteins with links to cell cycle control and apoptosis. However, the actual mechanism of IGFBP-3 action is still unclear. In an effort to clearly understand the mechanism of IGF-independent IGFBP-3 actions, a proteomic approach to identify the actual proteins involved in interaction with IGFBP-3 from different cell compartments, the phosphorylation status of IGFBP-3 under different physiologic conditions and the proteins upregulated by IGFBP-3 are briefly reviewed. The IGF system is a well-recognized key player in diseases such as cancer, diabetes and malnutrition. It is only after the signaling pathways of the IGF-independent actions of IGFBP-3 are clearly understood that the system can be manipulated to affect these disorders.
    MeSH term(s) Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Databases, Protein ; Humans ; Insulin-Like Growth Factor Binding Protein 3/physiology ; Neoplasms/blood ; Phosphorylation ; Protein Processing, Post-Translational ; Proteomics/methods ; Signal Transduction ; Somatomedins/physiology ; Spectrometry, Mass, Electrospray Ionization
    Chemical Substances Insulin-Like Growth Factor Binding Protein 3 ; Somatomedins
    Language English
    Publishing date 2005-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2299100-1
    ISSN 1744-8387 ; 1478-9450
    ISSN (online) 1744-8387
    ISSN 1478-9450
    DOI 10.1586/14789450.2.1.71
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Omalizumab reverses the phenotypic and functional effects of IgE-enhanced Fc epsilonRI on human skin mast cells.

    Gomez, Gregorio / Jogie-Brahim, Sherryline / Shima, Mika / Schwartz, Lawrence B

    Journal of immunology (Baltimore, Md. : 1950)

    2007  Volume 179, Issue 2, Page(s) 1353–1361

    Abstract: The dramatic effects of the anti-IgE mAb omalizumab to lower free IgE levels and Fc epsilonRI levels on basophils contrast with more modest clinical effects. Accordingly, whether IgE modulates Fc epsilonRI levels and Fc epsilonRI-dependent mediator ... ...

    Abstract The dramatic effects of the anti-IgE mAb omalizumab to lower free IgE levels and Fc epsilonRI levels on basophils contrast with more modest clinical effects. Accordingly, whether IgE modulates Fc epsilonRI levels and Fc epsilonRI-dependent mediator release in vitro on human skin mast cells (MC(TC) type) that had matured in vivo is of interest. IgE reversibly enhanced Fc epsilonRI levels on MC(TC) cells in a dose- and time-dependent manner (up-regulation t(1/2) of 4-5 days with 1-3 microg/ml IgE), without affecting cell proliferation. A molar ratio of omalizumab to IgE of 0.9 at baseline prevented receptor up-regulation by 50%, whereas adding omalizumab to MC(TC) cells already with IgE-enhanced Fc epsilonRI levels at molar ratios of 5, 12.5, and 31 reduced Fc epsilonRI levels to baseline with respective t(1/2) values of 8.7, 6.3, and 4.8 days. MC(TC) cells with IgE-enhanced Fc epsilonRI levels were more sensitive to stimulation with a low dose of anti-Fc epsilonRI mAb in terms of degranulation and production of PGD(2), GM-CSF, IL-6, IL-13, and TNF-alpha. Reducing up-regulated Fc epsilonRI levels with omalizumab also reduced mediator release to a low dose of anti-Fc epsilonRI mAb to baseline by 3-4 wk. Thus, reducing free IgE should decrease the hypersensitivity of allergic individuals to low naturally occurring concentrations of allergens.
    MeSH term(s) Anti-Allergic Agents/pharmacology ; Antibodies, Anti-Idiotypic ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal, Humanized ; Cell Degranulation/drug effects ; Cell Degranulation/immunology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Enzyme-Linked Immunosorbent Assay ; Humans ; Hypersensitivity/drug therapy ; Hypersensitivity/immunology ; Immunoglobulin E/drug effects ; Immunoglobulin E/immunology ; Mast Cells/drug effects ; Mast Cells/immunology ; Omalizumab ; Phenotype ; Receptors, IgE/immunology ; Skin/cytology ; Skin/drug effects ; Skin/immunology
    Chemical Substances Anti-Allergic Agents ; Antibodies, Anti-Idiotypic ; Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Receptors, IgE ; Omalizumab (2P471X1Z11) ; Immunoglobulin E (37341-29-0)
    Language English
    Publishing date 2007-02-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.179.2.1353
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    Ud II Zs.37: Show issues Location:
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  6. Article: Insulin-like growth factor-binding protein-3 suppresses tumor growth via activation of caspase-dependent apoptosis and cross-talk with NF-κB signaling

    Han, Jinfeng / Jogie-Brahim, Sherryline / Harada, Aki / Oh, Youngman

    Cancer letters. 2011 Aug. 28, v. 307, no. 2

    2011  

    Abstract: Nuclear factor-kappaB (NF-κB) is constitutively activated in a variety of human cancers including prostate cancer and involved in tumorigenesis, tumor progression and chemo-resistance. Insulin-like growth factor-binding protein-3 (IGFBP-3) is a potent ... ...

    Abstract Nuclear factor-kappaB (NF-κB) is constitutively activated in a variety of human cancers including prostate cancer and involved in tumorigenesis, tumor progression and chemo-resistance. Insulin-like growth factor-binding protein-3 (IGFBP-3) is a potent tumor suppressor and is significantly suppressed in a variety of cancers. Diverse biological effects of IGFBP-3 have been reported to be both dependent and independent of the IGF/IGF-I receptor (IGF-IR) axis. The precise underlying mechanisms of IGF/IGF-IR-independent, antiproliferative actions of IGFBP-3 are yet to be elucidated. We found an inverse correlation between NF-κB activity and IGFBP-3 expression during prostate cancer progression using an in vitro prostate cancer progression model. Restoration of IGFBP-3 resulted in significant inhibition of constitutively elevated NF-κB activity in prostate cancer cells. IGFBP-3 further inhibited the expression of NF-κB-regulated angiogenic factors such as VEGF and IL-8, and cell adhesion molecules, ICAM-1 and VCAM-1. This inhibitory action of IGFBP-3 was IGF/IGF-IR-independent since IGFBP-3 mutant devoid of IGF binding affinity had a similar inhibitory effect. We identified that IGFBP-3 degrades the key NF-κB regulatory molecules–IκBα and p65-NF-κB proteins through activation of caspase-8 and -3/-7, thereby inhibiting elevated NF-κB activity in prostate cancer. Finally intratumoral administration of IGFBP-3 resulted in significant tumor suppression as well as sensitization of antitumor effect of doxorubicin. Our findings indicate that IGFBP-3 exerts antitumor effects via IGF-independent mechanisms which involve activation of caspase-dependent apoptosis and cross-talk with NF-κB signaling. The use of IGFBP-3 as a cancer therapeutic with this distinctive suppression mechanism may offer alternate means to treat chemotherapy resistant tumors.
    Keywords apoptosis ; binding capacity ; carcinogenesis ; caspase-8 ; cell adhesion ; chemotherapy ; doxorubicin ; humans ; interleukin-8 ; models ; mutants ; prostatic neoplasms ; proteins
    Language English
    Dates of publication 2011-0828
    Size p. 200-210.
    Publishing place Elsevier Ireland Ltd
    Document type Article
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2011.04.004
    Database NAL-Catalogue (AGRICOLA)

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  7. Article ; Online: Insulin-like growth factor-binding protein-3 (IGFBP-3) blocks the effects of asthma by negatively regulating NF-κB signaling through IGFBP-3R-mediated activation of caspases.

    Lee, Yong-Chul / Jogie-Brahim, Sherryline / Lee, Dae-Yeol / Han, Jinfeng / Harada, Aki / Murphy, Liam J / Oh, Youngman

    The Journal of biological chemistry

    2011  Volume 286, Issue 20, Page(s) 17898–17909

    Abstract: Insulin-like growth factor-binding protein-3 (IGFBP-3) is a multifunctional protein known for modulating mitogenic and metabolic actions of IGFs as well as exerting a variety of biological actions not involving IGFs. Here, we show that IGFBP-3 blocks ... ...

    Abstract Insulin-like growth factor-binding protein-3 (IGFBP-3) is a multifunctional protein known for modulating mitogenic and metabolic actions of IGFs as well as exerting a variety of biological actions not involving IGFs. Here, we show that IGFBP-3 blocks specific physiological consequences of asthma in an IGF-independent manner in vitro and in vivo. IGFBP-3 treatment effectively reduced all physiological manifestations of asthma examined in vivo (airway hyper-responsiveness, cellular and pathological changes in bronchoalveolar lavage fluid and lung tissue, and expression of numerous proinflammatory molecules). These unique IGFBP-3 effects were further confirmed in IGFBP-3-transgenic mice, thus strengthening the notion of IGFBP-3 actions within the respiratory system. Using human epithelial cells, we demonstrated the following: 1) IGFBP-3 blocks TNF-α-induced expression of proinflammatory molecules; 2) IGFBP-3 attenuates the TNF-α-induced migratory response of eosinophils; and 3) IGFBP-3 negatively regulates TNF-α-induced expression of the key NF-κB regulatory molecules IκBα and p65-NF-κB at the post-translational level. We identified that IGFBP-3 degrades IκBα and p65-NF-κB proteins through IGFBP-3 receptor (IGFBP-3R)-mediated activation of caspases thereby inhibiting TNF-α-induced activation of NF-κB signaling cascades. This unique IGFBP-3/IGFBP-3R action was further confirmed by demonstrating complete inhibition of IGFBP-3 action in the presence of caspase inhibitors as well as IGFBP-3R siRNAs. Non-IGF-binding IGFBP-3 mutants further proved the IGF-independent action of IGFBP-3. Our findings indicate that IGFBP-3 inhibits airway inflammation and hyper-responsiveness via an IGF-independent mechanism that involves activation of IGFBP-3R signaling and cross-talk with NF-κB signaling. The IGFBP-3/IGFBP-3R system therefore plays a pivotal role in the pathogenesis of asthma and can serve as a newly identified potential therapeutic target for this debilitating disease.
    MeSH term(s) Animals ; Asthma/genetics ; Asthma/metabolism ; Caspases/genetics ; Caspases/metabolism ; Cell Line ; Cell Movement ; Enzyme Activation/genetics ; Eosinophils/metabolism ; Female ; Humans ; I-kappa B Proteins/genetics ; I-kappa B Proteins/metabolism ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor Binding Proteins/genetics ; Insulin-Like Growth Factor Binding Proteins/metabolism ; Male ; Mice ; Mice, Transgenic ; Mutation ; NF-KappaB Inhibitor alpha ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Signal Transduction ; Transcription Factor RelA/genetics ; Transcription Factor RelA/metabolism ; Tumor Necrosis Factor-alpha/biosynthesis ; Tumor Necrosis Factor-alpha/genetics
    Chemical Substances I-kappa B Proteins ; IGFBP-3R protein, human ; IGFBP3 protein, human ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor Binding Proteins ; NFKBIA protein, human ; Nfkbia protein, mouse ; RELA protein, human ; Receptors, Cell Surface ; Rela protein, mouse ; Transcription Factor RelA ; Tumor Necrosis Factor-alpha ; NF-KappaB Inhibitor alpha (139874-52-5) ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2011-03-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M111.231035
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Expression of alpha-tryptase and beta-tryptase by human basophils.

    Jogie-Brahim, Sherryline / Min, Hae-Ki / Fukuoka, Yoshihiro / Xia, Han-Zhang / Schwartz, Lawrence B

    The Journal of allergy and clinical immunology

    2004  Volume 113, Issue 6, Page(s) 1086–1092

    Abstract: Background: Alpha and beta-tryptase levels in serum are clinical tools for the evaluation of systemic anaphylaxis and systemic mastocytosis. Basophils and mast cells are known to produce these proteins.: Objective: The current study examines the ... ...

    Abstract Background: Alpha and beta-tryptase levels in serum are clinical tools for the evaluation of systemic anaphylaxis and systemic mastocytosis. Basophils and mast cells are known to produce these proteins.
    Objective: The current study examines the effect of the alpha,beta-tryptase genotype on basophil tryptase levels and the type of tryptase stored in these cells.
    Methods: Tryptase extracted from purified peripheral blood basophils from 20 subjects was examined by using ELISAs measuring mature and total tryptase and by using an enzymatic assay with tosyl-Gly-Pro-Lys-p-nitroanilide. Tryptase genotypes (4:0, 3:1, and 2:2 beta/alpha ratios) were assessed by using a hot-stop PCR technique with alpha,beta-tryptase-specific primers. Total alpha,beta-tryptase mRNA was measured by means of competitive RT-PCR, and ratios of alpha to beta-tryptase mRNA were measured by means of hot-stop RT-PCR.
    Results: Tryptase in all but one of the basophil preparations was mature and enzymatically active. Tryptase quantities in basophils were less than 1% of those in tissue mast cells. Tryptase genotypes (beta/alpha) among the 20 donors were 4:0 in 7, 3:1 in 7, and 2:2 in 6. Tryptase protein and mRNA levels per basophil were not affected by the tryptase genotype.
    Conclusion: Basophils from healthy subjects contain modest amounts of mature and enzymatically active tryptase unaffected by the tryptase genotype.
    MeSH term(s) Basophils/enzymology ; Cell Line ; Genotype ; Humans ; RNA, Messenger/analysis ; Reverse Transcriptase Polymerase Chain Reaction ; Serine Endopeptidases/analysis ; Serine Endopeptidases/genetics ; Tryptases
    Chemical Substances RNA, Messenger ; Serine Endopeptidases (EC 3.4.21.-) ; Tryptases (EC 3.4.21.59)
    Language English
    Publishing date 2004-06
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 121011-7
    ISSN 1085-8725 ; 1097-6825 ; 0091-6749
    ISSN (online) 1085-8725 ; 1097-6825
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2004.02.032
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Insulin-like growth factor-binding protein-3 suppresses tumor growth via activation of caspase-dependent apoptosis and cross-talk with NF-κB signaling

    Han, Jinfeng / Jogie-Brahim, Sherryline / Harada, Aki / Oh, Youngman

    Cancer letters

    Volume v. 307,, Issue no. 2

    Abstract: Nuclear factor-kappaB (NF-κB) is constitutively activated in a variety of human cancers including prostate cancer and involved in tumorigenesis, tumor progression and chemo-resistance. Insulin-like growth factor-binding protein-3 (IGFBP-3) is a potent ... ...

    Abstract Nuclear factor-kappaB (NF-κB) is constitutively activated in a variety of human cancers including prostate cancer and involved in tumorigenesis, tumor progression and chemo-resistance. Insulin-like growth factor-binding protein-3 (IGFBP-3) is a potent tumor suppressor and is significantly suppressed in a variety of cancers. Diverse biological effects of IGFBP-3 have been reported to be both dependent and independent of the IGF/IGF-I receptor (IGF-IR) axis. The precise underlying mechanisms of IGF/IGF-IR-independent, antiproliferative actions of IGFBP-3 are yet to be elucidated. We found an inverse correlation between NF-κB activity and IGFBP-3 expression during prostate cancer progression using an in vitro prostate cancer progression model. Restoration of IGFBP-3 resulted in significant inhibition of constitutively elevated NF-κB activity in prostate cancer cells. IGFBP-3 further inhibited the expression of NF-κB-regulated angiogenic factors such as VEGF and IL-8, and cell adhesion molecules, ICAM-1 and VCAM-1. This inhibitory action of IGFBP-3 was IGF/IGF-IR-independent since IGFBP-3 mutant devoid of IGF binding affinity had a similar inhibitory effect. We identified that IGFBP-3 degrades the key NF-κB regulatory molecules–IκBα and p65-NF-κB proteins through activation of caspase-8 and -3/-7, thereby inhibiting elevated NF-κB activity in prostate cancer. Finally intratumoral administration of IGFBP-3 resulted in significant tumor suppression as well as sensitization of antitumor effect of doxorubicin. Our findings indicate that IGFBP-3 exerts antitumor effects via IGF-independent mechanisms which involve activation of caspase-dependent apoptosis and cross-talk with NF-κB signaling. The use of IGFBP-3 as a cancer therapeutic with this distinctive suppression mechanism may offer alternate means to treat chemotherapy resistant tumors.
    Keywords doxorubicin ; apoptosis ; humans ; prostatic neoplasms ; chemotherapy ; caspase-8 ; interleukin-8 ; mutants ; models ; carcinogenesis ; cell adhesion ; proteins ; binding capacity
    Language English
    Document type Article
    ISSN 0304-3835
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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