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New Findings on Cancer Gene Therapy from J. Bieniek and Co-Authors Summarized (COX-2 inhibitors Arrest Prostate Cancer Cell Cycle Progression by...

July 28, 2014



New Findings on Cancer Gene Therapy from J. Bieniek and Co-Authors Summarized (COX-2 inhibitors Arrest Prostate Cancer Cell Cycle Progression by Down-Regulation of Kinetochore/Centromere Proteins)

By a News Reporter-Staff News Editor at Cancer Gene Therapy Week -- New research on Biotechnology is the subject of a report. According to news reporting from Danville, Pennsylvania, by NewsRx journalists, research stated, "Previous studies have shown that COX-2 inhibitors inhibit cancer cell proliferation. However, the molecular mechanism remains elusive."

The news correspondents obtained a quote from the research, "Prostate cancer LNCaP, 22Rv1, and PC3 cells were cultured and treated with the COX-2 inhibitors celecoxib and CAY10404. Knockdown of COX-2 in LNCaP cells was carried out using lentiviral vector-loaded COX-2 shRNA. Cell cycle progression and cell proliferation were analyzed by flow cytometry, microscopy, cell counting, and the MTT assay. The antagonists of EP1, EP2, EP3, and EP4 were used to examine the effects of the PGE2 signaling. The effect of COX-2 inhibitors and COX-2 knockdown on expression of the kinetochore/centromere genes and proteins was determined by RT-PCR and immunoblotting. Treatment with the COX-2 inhibitors celecoxib and CAY10404 or knockdown of COX-2 significantly inhibited prostate cancer cell proliferation. Flow-cytometric analysis and immunofluorescent staining confirmed the cell cycle arrested at the G2/M phase. Biochemical analysis showed that inhibition of COX-2 or suppression of COX-2 expression induced a dramatic down-regulation of key proteins in the kinetochore/centromere assembly, such as ZWINT, Cdc20, Ndc80, CENP-A, Bub1, and Plk1. Furthermore, the EP1 receptor antagonist SC51322, but not the EP2, EP3, and EP4 receptor antagonists, produced similar effects to the COX-2 inhibitors on cell proliferation and down-regulation of kinetochore/centromere proteins, suggesting that the effect of the COX-2 inhibition is through inactivation of the EP1 receptor signaling."

According to the news reporters, the research concluded: "Our studies indicate that inhibition of COX-2 can arrest prostate cancer cell cycle progression through inactivation of the EP1 receptor signaling and down-regulation of kinetochore/centromere proteins."

For more information on this research see: COX-2 inhibitors Arrest Prostate Cancer Cell Cycle Progression by Down-Regulation of Kinetochore/Centromere Proteins. Prostate, 2014;74(10):999-1011. Prostate can be contacted at: Wiley-Blackwell, 111 River St, Hoboken 07030-5774, NJ, USA. (Wiley-Blackwell - www.wiley.com/; Prostate - onlinelibrary.wiley.com/journal/10.1002/(ISSN)1097-0045)

Our news journalists report that additional information may be obtained by contacting J. Bieniek, Geisinger Med Clin, Weis Center Res, Danville, PA 17822, United States. Additional authors for this research include C. Childress, M.D. Swatski and W.N. Yang (see also Biotechnology).

Keywords for this news article include: Danville, Pennsylvania, United States, North and Central America, Amino Acids, Biotechnology, Cancer Gene Therapy, Cell Nucleus Structures, Cell Proliferation, Centromere, Chromosome Structures, Chromosomes, Genetics, Intranuclear Space, Kinetochores, Oncology, Peptides, Prostate Cancer, Prostatic Neoplasms, Proteins

Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2014, NewsRx LLC


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Source: Cancer Gene Therapy Week


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