Reports from H. Lee Moffitt Cancer Center and Research Institute Highlight Recent Research in Pancreatic Cancer
By a News Reporter-Staff News Editor at Gastroenterology Week -- A new study on Pancreatic Cancer is now available. According to news originating from Tampa, Florida, by NewsRx correspondents, research stated, "Vitamin E d-tocotrienol has been shown to have antitumor activity, but the precise molecular mechanism by which it inhibits the proliferation of cancer cells remains unclear. Here, we demonstrated that d-tocotrienol exerted significant cell growth inhibition pancreatic ductal cancer (PDCA) cells without affecting normal human pancreatic ductal epithelial cell growth."
Our news journalists obtained a quote from the research from H. Lee Moffitt Cancer Center and Research Institute, "We also showed that d-tocotrienol-induced growth inhibition occurred concomitantly with G(1) cell-cycle arrest and increased p27(Kip1) nuclear accumulation. This finding is significant considering that loss of nuclear p27(Kip1) expression is a well-established adverse prognostic factor in PDCA. Furthermore, d-tocotrienol inactivated RAF-MEK-ERK signaling, a pathway known to suppress p27(Kip1) expression. To determine whether p27(Kip1) induction is required for d-tocotrienol inhibition of PDCA cell proliferation, we stably silenced the CDKN1B gene, encoding p27(Kip1), in MIAPaCa-2 PDCA cells and demonstrated that p27(Kip1) silencing suppressed cell-cycle arrest induced by d-tocotrienol. Furthermore, d-tocotrienol induced p27(Kip1) mRNA expression but not its protein degradation. p27(Kip1) gene promoter activity was induced by d-tocotrienol through the promoter's E2F-1 binding site, and this activity was attenuated by E2F-1 depletion using E2F-1 small interfering RNA. Finally, decreased proliferation, mediated by Ki67 and p27(Kip1) expression by d-tocotrienol, was confirmed in vivo in a nude mouse xenograft pancreatic cancer model."
According to the news editors, the research concluded: "Our findings reveal a new mechanism, dependent on p27(Kip1) induction, by which d-tocotrienol can inhibit proliferation in PDCA cells, providing a new rationale for p27(Kip1) as a biomarker for d-tocotrienol efficacy in pancreatic cancer prevention and therapy."
For more information on this research see: Vitamin E d-Tocotrienol Induces p27(Kip1)-Dependent Cell-Cycle Arrest in Pancreatic Cancer Cells via an E2F-1-Dependent Mechanism. Plos One, 2013;8(2):e52526. (Public Library of Science - www.plos.org; Plos One - www.plosone.org)
The news correspondents report that additional information may be obtained from P.J. Hodul, Dept. of Gastrointestinal Oncology, H Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, United States (see also Pancreatic Cancer).
Keywords for this news article include: Tampa, Florida, Oncology, United States, Gastroenterology, Pancreatic Cancer, Risk and Prevention, Pancreatic Neoplasms, North and Central America.
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