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max schmidt & jian-ting zhang michele yip-schneider cell cycle profiles open access article pre-publication history article download pdf dna double-strand break fresh-frozen tissues combined histological type-specific inactivation jian-ting zhang full-length 115-kda protein resisting drug-induced apoptosis survive dna-damaging treatments pancreatic ductal adenocarcinoma fresh frozen tissues differentially expressed growth vector-transfected control cells control vector-transfected cells authors’ original file dna-damage induced apoptosis cell cycle progression privacy choices/manage cookies pancreatic cancer patients basal/myoepithelial phenotypes pancreatic cancer tissues cancer pancreatic tissues drug-induced parp cleavage fresh-frozen normal full size image cell growth differ anti-neoplastic effects cyclin-dependent kinases human pancreatic cancers pancreatic cancer cells vec-transfected control cells lung cancer tissues van heusden gp van heek nt negatively regulates bax cell cycle distribution intestinal cell differentiation view induce cell death author correspondence cell cycle regulation human lung cancers indiana university school kaplan-meier method bmc cancer 10 mol cell proteomics

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         headline:Role of 14-3-3σ in poor prognosis and in radiation and drug resistance of human pancreatic cancers
         description:Pancreatic cancer is the fourth leading cause of death in the US. Unlike other solid tumors such as testicular cancer which are now curable, more than 90% of pancreatic cancer patients die due to lack of response to therapy. Recently, the level of 14-3-3σ mRNA was found to be increased in pancreatic cancers and this increased expression may contribute to the failure in treatment of pancreatic cancers. In the present study, we tested this hypothesis. Western blot analysis was used to determine 14-3-3σ protein level in fresh frozen tissues and was correlated to clinical outcome. A stable cell line expressing 14-3-3σ was established and the effect of 14-3-3σ over-expression on cellular response to radiation and anticancer drugs were tested using SRB assay and clonogenic assays. Cell cycle distribution and apoptosis analyses were performed using propidium iodide staining and PARP cleavage assays. We found that 14-3-3σ protein level was increased significantly in about 71% (17 of 24) of human pancreatic cancer tissues and that the 14-3-3σ protein level in cancers correlated with lymph node metastasis and poor prognosis. Furthermore, we demonstrated that over-expression of 14-3-3σ in a pancreatic cancer cell line caused resistance to γ-irradiation as well as anticancer drugs by causing resistance to treatment-induced apoptosis and G2/M arrest. The increased level of 14-3-3σ protein likely contributes to the poor clinical outcome of human pancreatic cancers by causing resistance to radiation and anticancer drugs. Thus, 14-3-3σ may serve as a prognosis marker predicting survival of pancreatic cancer patients and guide the clinical treatment of these patients.
         datePublished:2010-11-01T00:00:00Z
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            Gemcitabine
            Pancreatic Cancer Cell
            Mitoxantrone
            Human Pancreatic Cancer
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
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      headline:Role of 14-3-3σ in poor prognosis and in radiation and drug resistance of human pancreatic cancers
      description:Pancreatic cancer is the fourth leading cause of death in the US. Unlike other solid tumors such as testicular cancer which are now curable, more than 90% of pancreatic cancer patients die due to lack of response to therapy. Recently, the level of 14-3-3σ mRNA was found to be increased in pancreatic cancers and this increased expression may contribute to the failure in treatment of pancreatic cancers. In the present study, we tested this hypothesis. Western blot analysis was used to determine 14-3-3σ protein level in fresh frozen tissues and was correlated to clinical outcome. A stable cell line expressing 14-3-3σ was established and the effect of 14-3-3σ over-expression on cellular response to radiation and anticancer drugs were tested using SRB assay and clonogenic assays. Cell cycle distribution and apoptosis analyses were performed using propidium iodide staining and PARP cleavage assays. We found that 14-3-3σ protein level was increased significantly in about 71% (17 of 24) of human pancreatic cancer tissues and that the 14-3-3σ protein level in cancers correlated with lymph node metastasis and poor prognosis. Furthermore, we demonstrated that over-expression of 14-3-3σ in a pancreatic cancer cell line caused resistance to γ-irradiation as well as anticancer drugs by causing resistance to treatment-induced apoptosis and G2/M arrest. The increased level of 14-3-3σ protein likely contributes to the poor clinical outcome of human pancreatic cancers by causing resistance to radiation and anticancer drugs. Thus, 14-3-3σ may serve as a prognosis marker predicting survival of pancreatic cancer patients and guide the clinical treatment of these patients.
      datePublished:2010-11-01T00:00:00Z
      dateModified:2010-11-01T00:00:00Z
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         Pancreatic Cancer
         Gemcitabine
         Pancreatic Cancer Cell
         Mitoxantrone
         Human Pancreatic Cancer
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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