Arachidonoyl-ethanolamide activates endoplasmic reticulum stress-apoptosis in tumorigenic keratinocytes: Role of cyclooxygenase-2 and novel J-series prostamides.

Faculty Pharmacy Year: 2016
Type of Publication: ZU Hosted Pages:
Authors:
Eman Salah Abdelaziz Souliman
Journal: molecular carcinogenesis wiley online library Volume:
Keywords : Arachidonoyl-ethanolamide activates endoplasmic reticulum stress-apoptosis , tumorigenic    
Abstract:
Non-melanoma skin cancer and other epithelial tumors overexpress cyclooxygenase-2 (COX-2), differentiating them from normal cells. COX-2 metabolizes arachidonic acid to prostaglandins including, the J-series prostaglandins, which induce apo
    
     
 
       

Author Related Publications

  • Eman Salah Abdelaziz Souliman, "Synthesis and Evaluation of the Novel Prostamide, 15-Deoxy, Δ12,14-Prostamide J2, as a Selective Antitumor Therapeutic", American Associatiion of Cancer Research, 2017 More
  • Eman Salah Abdelaziz Souliman, "Cannabinoids Modulate Neuronal Activity and Cancer by CB1 and CB2 Receptor-Independent Mechanisms", Experimental Pharmacology and drug discovery, 2017 More
  • Eman Salah Abdelaziz Souliman, "Receptor-dependent and receptor-independent endocannabinoid signaling: a therapeutic target for regulation of cancer growth.", Elsevier, 2013 More
  • Eman Salah Abdelaziz Souliman, "Anandamide-induced endoplasmic reticulum stress and apoptosis are mediated by oxidative stress in non-melanoma skin cancer: Receptor-independent endocannabinoid signaling.", wiley online library, 2016 More
  • Eman Salah Abdelaziz Souliman, "Apigenin inhibits COX-2, PGE2, and EP1 and also initiates terminal differentiation in the epidermis of tumor bearing mice.", Elsevier, 2016 More

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