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  1. AU="Carter, Jada R"
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  1. Artikel ; Online: Serum deprivation initiates adaptation and survival to oxidative stress in prostate cancer cells.

    White, ElShaddai Z / Pennant, Nakea M / Carter, Jada R / Hawsawi, Ohuod / Odero-Marah, Valerie / Hinton, Cimona V

    Scientific reports

    2020  Band 10, Heft 1, Seite(n) 12505

    Abstract: Inadequate nutrient intake leads to oxidative stress disrupting homeostasis, activating signaling, and altering metabolism. Oxidative stress serves as a hallmark in developing prostate lesions, and an aggressive cancer phenotype activating mechanisms ... ...

    Abstract Inadequate nutrient intake leads to oxidative stress disrupting homeostasis, activating signaling, and altering metabolism. Oxidative stress serves as a hallmark in developing prostate lesions, and an aggressive cancer phenotype activating mechanisms allowing cancer cells to adapt and survive. It is unclear how adaptation and survival are facilitated; however, literature across several organisms demonstrates that a reversible cellular growth arrest and the transcription factor, nuclear factor-kappaB (NF-κB), contribute to cancer cell survival and therapeutic resistance under oxidative stress. We examined adaptability and survival to oxidative stress following nutrient deprivation in three prostate cancer models displaying varying degrees of tumorigenicity. We observed that reducing serum (starved) induced reactive oxygen species which provided an early oxidative stress environment and allowed cells to confer adaptability to increased oxidative stress (H
    Mesh-Begriff(e) Adaptation, Physiological/drug effects ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Culture Media, Serum-Free ; Humans ; Male ; NF-kappa B/metabolism ; Oxidative Stress/drug effects ; Phenotype ; Prostatic Neoplasms/pathology ; Protein Transport/drug effects
    Chemische Substanzen Antineoplastic Agents ; Culture Media, Serum-Free ; NF-kappa B
    Sprache Englisch
    Erscheinungsdatum 2020-07-27
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-68668-x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Agonist-induced CXCR4 and CB2 Heterodimerization Inhibits Gα13/RhoA-mediated Migration.

    Scarlett, Kisha A / White, El-Shaddai Z / Coke, Christopher J / Carter, Jada R / Bryant, Latoya K / Hinton, Cimona V

    Molecular cancer research : MCR

    2018  Band 16, Heft 4, Seite(n) 728–739

    Abstract: G-protein-coupled receptor (GPCR) heterodimerization has emerged as a means by which alternative signaling entities can be created; yet, how receptor heterodimers affect receptor pharmacology remains unknown. Previous observations suggested a biochemical ...

    Abstract G-protein-coupled receptor (GPCR) heterodimerization has emerged as a means by which alternative signaling entities can be created; yet, how receptor heterodimers affect receptor pharmacology remains unknown. Previous observations suggested a biochemical antagonism between GPCRs, CXCR4 and CB2 (CNR2), where agonist-bound CXCR4 and agonist-bound CB2 formed a physiologically nonfunctional heterodimer on the membrane of cancer cells, inhibiting their metastatic potential
    Mesh-Begriff(e) Cannabinoids/pharmacology ; Cell Adhesion/drug effects ; Cell Line, Tumor ; Cell Movement/drug effects ; Chemokine CXCL12/metabolism ; Down-Regulation ; Female ; GTP-Binding Protein alpha Subunits, G12-G13/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; HEK293 Cells ; Heterocyclic Compounds/pharmacology ; Humans ; Male ; Neoplasms/metabolism ; PC-3 Cells ; Receptor, Cannabinoid, CB2/agonists ; Receptor, Cannabinoid, CB2/metabolism ; Receptors, CXCR4/agonists ; Receptors, CXCR4/metabolism ; rhoA GTP-Binding Protein/metabolism
    Chemische Substanzen AM 1241 ; CNR2 protein, human ; CXCL12 protein, human ; CXCR4 protein, human ; Cannabinoids ; Chemokine CXCL12 ; GNA13 protein, human ; Heterocyclic Compounds ; Receptor, Cannabinoid, CB2 ; Receptors, CXCR4 ; RHOA protein, human (124671-05-2) ; GTP-Binding Protein alpha Subunits, G12-G13 (EC 3.6.5.1) ; rhoA GTP-Binding Protein (EC 3.6.5.2) ; plerixafor (S915P5499N)
    Sprache Englisch
    Erscheinungsdatum 2018-01-12
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-16-0481
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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