LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 2 of total 2

Search options

  1. Article ; 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  Volume 10, Issue 1, Page(s) 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 term(s) 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
    Chemical Substances Antineoplastic Agents ; Culture Media, Serum-Free ; NF-kappa B
    Language English
    Publishing date 2020-07-27
    Publishing country England
    Document type 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; 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  Volume 16, Issue 4, Page(s) 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 term(s) 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
    Chemical Substances 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)
    Language English
    Publishing date 2018-01-12
    Publishing country United States
    Document type 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top