title: Novel antineoplastic isochalcones inhibit the expression of cyclooxygenase 1,2 and EGF in human prostate cancer cell line LNCaP.
abstract: Experiments were conducted to determine the effects of novel anti-neoplastic isochalcones (DJ compounds), on cyclooxyegenase 1 and 2 (COX-1 and COX-2) enzyme expression in androgen receptor dependent human prostate cancer cell line LNCaP. Results from Western blot analysis and cell flow cytometry showed that DJ52 and DJ53 decreased the steady state levels of COX-1 and COX-2 protein levels in a dose dependent manner. In addition, DJ52 and DJ53 decreased the levels of epidermal growth factor (EGF) in LNCaP cells. In this study, we report that novel isochalcones decreased COX-1, COX-2 and EGF levels as well as LNCaP cellular growth in a dose responsive manner. Our findings indicate that relative decreases in COX-1, COX-2 and EGF expressions might serve as indicators of tumor growth inhibition in prostate neoplasms.
authors.affiliation: Department of Biology, Clark Atlanta University, Morehouse College, Georgia 30314, USA.
authors.forename: K P
authors.initials: KP
authors.lastname: Johnson
authors.forename: G C
authors.initials: GC
authors.lastname: Rowe
authors.forename: B A
authors.initials: BA
authors.lastname: Jackson
authors.forename: J L
authors.initials: JL
authors.lastname: D'Agustino
authors.forename: P E
authors.initials: PE
authors.lastname: Campbell
authors.forename: B O
authors.initials: BO
authors.lastname: Guillory
authors.forename: M V
authors.initials: MV
authors.lastname: Williams
authors.forename: Q L
authors.initials: QL
authors.lastname: Matthews
authors.forename: J
authors.initials: J
authors.lastname: McKay
authors.forename: G M
authors.initials: GM
authors.lastname: Charles
authors.forename: C R
authors.initials: CR
authors.lastname: Verret
authors.forename: M
authors.initials: M
authors.lastname: Deleon
authors.forename: D E
authors.initials: DE
authors.lastname: Johnson
authors.forename: D B
authors.initials: DB
authors.lastname: Cooke
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D002455:Cell Division / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D004305:Dose-Response Relationship, Drug; D004815:Epidermal Growth Factor / Q000378:metabolism*; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D066246:ErbB Receptors / Q000502:physiology; D018120:Finasteride / Q000494:pharmacology; D006131:Growth Inhibitors / Q000494:pharmacology*; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D011467:Prostate / Q000166:cytology; D011471:Prostatic Neoplasms / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D011944:Receptors, Androgen / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D000970:Antineoplastic Agents; D006131:Growth Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D011944:Receptors, Androgen; D018120:Finasteride; D004815:Epidermal Growth Factor; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496511:PTGS1 protein, human; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D066246:ErbB Receptors