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  1. Artikel ; Online: Pantoprazole Induces Mitochondrial Apoptosis and Attenuates NF-κB Signaling in Glioma Cells.

    Geeviman, Khamushavalli / Babu, Deepak / Prakash Babu, Phanithi

    Cellular and molecular neurobiology

    2018  Band 38, Heft 8, Seite(n) 1491–1504

    Abstract: ... Gastric ... ...

    Abstract Gastric H
    Mesh-Begriff(e) Animals ; Apoptosis/drug effects ; Caspase 3/metabolism ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Glioma/metabolism ; Glioma/pathology ; Humans ; Membrane Potential, Mitochondrial/drug effects ; Mitochondria/drug effects ; Mitochondria/metabolism ; NF-kappa B/metabolism ; Pantoprazole/pharmacology ; Poly(ADP-ribose) Polymerases/metabolism ; Rats ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Time Factors ; Transcription Factor RelA/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
    Chemische Substanzen NF-kappa B ; RELA protein, human ; Reactive Oxygen Species ; Transcription Factor RelA ; Tumor Necrosis Factor-alpha ; Pantoprazole (D8TST4O562) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; Caspase 3 (EC 3.4.22.-)
    Sprache Englisch
    Erscheinungsdatum 2018-10-09
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 283404-2
    ISSN 1573-6830 ; 0272-4340
    ISSN (online) 1573-6830
    ISSN 0272-4340
    DOI 10.1007/s10571-018-0623-4
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1727: Hefte anzeigen Standort:
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  2. Artikel ; Online: The nonsteroidal anti-inflammatory drug celecoxib suppresses the growth and induces apoptosis of human glioblastoma cells via the NF-κB pathway.

    Sareddy, Gangadhara Reddy / Geeviman, Khamushavalli / Ramulu, Chinta / Babu, Phanithi Prakash

    Journal of neuro-oncology

    2011  Band 106, Heft 1, Seite(n) 99–109

    Abstract: Gliomas are devastating primary tumors of the central nervous system and tend to recur even after standard therapy. Celecoxib, the selective COX-2 nonsteroidal anti-inflammatory drug, has anti-neoplastic activity against several malignancies. ... ...

    Abstract Gliomas are devastating primary tumors of the central nervous system and tend to recur even after standard therapy. Celecoxib, the selective COX-2 nonsteroidal anti-inflammatory drug, has anti-neoplastic activity against several malignancies. Accumulating evidence suggests that several COX-2-independent mechanisms may also be involved in the anti-tumor effects of celecoxib. Deregulation of the NF-κB signaling pathway contributes to enhanced glioma cell survival, proliferation, and chemoresistance. In this study, we examined the efficacy of celecoxib in suppressing the growth of glioblastoma cell lines. We observed that treatment with celecoxib significantly reduced the proliferation of a variety of GBM cell lines in a dose-dependent manner and also induced apoptosis, which was evident from enhanced caspase-3 and 8 activity, PARP cleavage, and TUNEL positive cells. Celecoxib treatment significantly down-regulated TNF-α induced NF-κB nuclear translocation, NF-κB DNA binding activity, and NF-κB-dependent reporter gene expression in U373 and T98G cells in a dose-dependent manner. Furthermore, celecoxib suppressed IκBα degradation and phosphorylation and reduced IKK activity in a dose-dependent manner. This study provides evidence that celecoxib suppresses the growth of GBM cell lines partly by inhibiting the NF-κB signaling pathway.
    Mesh-Begriff(e) Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Apoptosis/drug effects ; Blotting, Western ; Brain Neoplasms/drug therapy ; Brain Neoplasms/pathology ; Celecoxib ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cell Survival/drug effects ; Colony-Forming Units Assay ; Coloring Agents ; Cyclooxygenase 2 Inhibitors/pharmacology ; Cytosol/metabolism ; Dose-Response Relationship, Drug ; Electrophoretic Mobility Shift Assay ; Fluorescent Antibody Technique ; Glioblastoma/drug therapy ; Glioblastoma/pathology ; Humans ; I-kappa B Proteins/metabolism ; In Situ Nick-End Labeling ; NF-kappa B/physiology ; Protein Transport ; Pyrazoles/pharmacology ; Signal Transduction/drug effects ; Sulfonamides/pharmacology ; Tetrazolium Salts ; Thiazoles ; Tumor Necrosis Factor-alpha/antagonists & inhibitors
    Chemische Substanzen Anti-Inflammatory Agents, Non-Steroidal ; Coloring Agents ; Cyclooxygenase 2 Inhibitors ; I-kappa B Proteins ; NF-kappa B ; Pyrazoles ; Sulfonamides ; Tetrazolium Salts ; Thiazoles ; Tumor Necrosis Factor-alpha ; thiazolyl blue (EUY85H477I) ; Celecoxib (JCX84Q7J1L)
    Sprache Englisch
    Erscheinungsdatum 2011-08-17
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604875-4
    ISSN 1573-7373 ; 0167-594X
    ISSN (online) 1573-7373
    ISSN 0167-594X
    DOI 10.1007/s11060-011-0662-x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1825: Hefte anzeigen Standort:
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  3. Artikel ; Online: Increased β-catenin/Tcf signaling in pilocytic astrocytomas: a comparative study to distinguish pilocytic astrocytomas from low-grade diffuse astrocytomas.

    Sareddy, Gangadhara Reddy / Geeviman, Khamushavalli / Panigrahi, Manas / Challa, Sundaram / Mahadevan, Anita / Babu, Phanithi Prakash

    Neurochemical research

    2011  Band 37, Heft 1, Seite(n) 96–104

    Abstract: Although pilocytic and diffuse grade II astrocytomas considered as low-grade tumors, the distinction between them is still a major clinical problem. Previously we reported the activation of Wnt/β-catenin/Tcf signaling pathway in diffuse astrocytomas, ... ...

    Abstract Although pilocytic and diffuse grade II astrocytomas considered as low-grade tumors, the distinction between them is still a major clinical problem. Previously we reported the activation of Wnt/β-catenin/Tcf signaling pathway in diffuse astrocytomas, however its role in pilocytic astrocytomas is not well understood. In this study, we investigated the Wnt/β-catenin/Tcf pathway in pilocytic astrocytomas and compared with diffuse astrocytomas. We observed the differential expression of β-catenin, Tcf4, Lef1 and c-Myc in astrocytomas particularly higher levels were observed in pilocytic astrocytomas and GBM while very little expression was documented in grade II tumors. Further, immunohistochemical analysis revealed the strong positivity of β-catenin, Tcf4, Lef1 and c-Myc in pilocytic astrocytomas than that of grade II tumors and also exhibited the strong positivity in vascular endothelial cells of pilocytic astrocytomas and GBM. Hence, Wnt/β-catenin/Tcf signaling pathway is differentially expressed in astrocytomas, activation of this pathway might be helpful in separating pilocytic astrocytomas from low-grade diffuse astrocytomas.
    Mesh-Begriff(e) Adolescent ; Adult ; Astrocytoma/metabolism ; Astrocytoma/pathology ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Child ; Child, Preschool ; Female ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Signal Transduction ; TCF Transcription Factors/metabolism ; beta Catenin/metabolism
    Chemische Substanzen TCF Transcription Factors ; beta Catenin
    Sprache Englisch
    Erscheinungsdatum 2011-09-16
    Erscheinungsland United States
    Dokumenttyp Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 199335-5
    ISSN 1573-6903 ; 0364-3190
    ISSN (online) 1573-6903
    ISSN 0364-3190
    DOI 10.1007/s11064-011-0586-z
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1368: Hefte anzeigen Standort:
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