Literature DB >> 15183989

c-FLIP expression in bladder urothelial carcinomas: its role in resistance to Fas-mediated apoptosis and clinicopathologic correlations.

Penelope Korkolopoulou1, Athina Goudopoulou, Gerassimos Voutsinas, Euphemia Thomas-Tsagli, Panagiotis Kapralos, Efstratios Patsouris, Angelica A Saetta.   

Abstract

OBJECTIVES: To investigate the incidence of Fas (exon 9) mutations and the expression of Fas, Fas-Fas ligand (FasL) system, and cellular FLICE-like inhibitory protein (c-FLIP) in relation to standard clinicopathologic parameters and patient outcome in bladder carcinoma. Disruption of apoptotic cell death has been implicated in tumor aggressiveness in bladder urothelial carcinomas. The FasL system is involved in the execution of apoptosis induced by the immune system. c-FLIP protein constitutes an important endogenous inhibitor of Fas and other death receptor-mediated apoptosis.
METHODS: The expression of Fas, FasL, and c-FLIP was quantified immunohistochemically in paraffin-embedded tissues from 53 patients for whom clinical information was available. DNA extracted from the same samples was screened for mutations in Fas exon 9 by single-strand conformation polymorphism and sequencing. The effect of Fas, FasL, and c-FLIP on clinical outcome was assessed by univariate and multivariate analyses.
RESULTS: Positive immunostaining was detected for Fas, FasL, and c-FLIP in 72%, 66%, and 81% of cases, respectively. Concurrent expression of Fas and FasL was seen in 27 samples (51%), of which 22 (81.5%) also displayed c-FLIP positivity. FasL and c-FLIP expression increased with advancing stage but was absent from normal urothelium. None of the 53 urothelial carcinoma samples analyzed showed evidence of mutations by polymerase chain reaction single-strand conformation polymorphism and direct sequencing. Survival analysis demonstrated that although both FasL and c-FLIP expression adversely affected survival, only c-FLIP remained statistically significant on multivariate analysis.
CONCLUSIONS: The frequent expression and coexpression of Fas, FasL, and c-FLIP in urothelial carcinomas implicates c-FLIP as an inhibitor of the Fas-FasL-induced death pathway in these tumors. Moreover, c-FLIP conveys independent prognostic information in the presence of classical prognosticators.

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Year:  2004        PMID: 15183989     DOI: 10.1016/j.urology.2004.01.007

Source DB:  PubMed          Journal:  Urology        ISSN: 0090-4295            Impact factor:   2.649


  24 in total

1.  The histone deacetylase inhibitor, MS-275 (entinostat), downregulates c-FLIP, sensitizes osteosarcoma cells to FasL, and induces the regression of osteosarcoma lung metastases.

Authors:  Krithi Rao-Bindal; Nadezhda V Koshkina; John Stewart; Eugenie S Kleinerman
Journal:  Curr Cancer Drug Targets       Date:  2013-05       Impact factor: 3.428

2.  Tumor necrosis factor (TNF) receptor-associated factor 7 is required for TNFα-induced Jun NH2-terminal kinase activation and promotes cell death by regulating polyubiquitination and lysosomal degradation of c-FLIP protein.

Authors:  Ivan Scudiero; Tiziana Zotti; Angela Ferravante; Mariangela Vessichelli; Carla Reale; Maria C Masone; Antonio Leonardi; Pasquale Vito; Romania Stilo
Journal:  J Biol Chem       Date:  2012-01-03       Impact factor: 5.157

3.  KSR1 is overexpressed in endometrial carcinoma and regulates proliferation and TRAIL-induced apoptosis by modulating FLIP levels.

Authors:  David Llobet; Nuria Eritja; Monica Domingo; Laura Bergada; Cristina Mirantes; Maria Santacana; Judit Pallares; Anna Macià; Andree Yeramian; Mario Encinas; Gema Moreno-Bueno; Jose Palacios; Robert E Lewis; Xavier Matias-Guiu; Xavi Dolcet
Journal:  Am J Pathol       Date:  2011-04       Impact factor: 4.307

4.  Expression of c-FLIP in pulmonary metastases in osteosarcoma patients and human xenografts.

Authors:  Krithi Rao-Bindal; Chethan K Rao; Ling Yu; Eugenie S Kleinerman
Journal:  Pediatr Blood Cancer       Date:  2012-12-19       Impact factor: 3.167

Review 5.  c-FLIP, a master anti-apoptotic regulator.

Authors:  A R Safa
Journal:  Exp Oncol       Date:  2012-10

6.  The Fas death signaling pathway connecting reactive oxygen species generation and FLICE inhibitory protein down-regulation.

Authors:  Liying Wang; Neelam Azad; Lalana Kongkaneramit; Fei Chen; Yongju Lu; Bing-Hua Jiang; Yon Rojanasakul
Journal:  J Immunol       Date:  2008-03-01       Impact factor: 5.422

7.  Involvement of FLIP in 2-methoxyestradiol-induced tumor regression in transgenic adenocarcinoma of mouse prostate model.

Authors:  Manonmani Ganapathy; Rita Ghosh; Xie Jianping; Xiaoping Zhang; Roble Bedolla; John Schoolfield; I-Tien Yeh; Dean A Troyer; Aria F Olumi; Addanki P Kumar
Journal:  Clin Cancer Res       Date:  2009-02-17       Impact factor: 12.531

Review 8.  The Histone Deacetylase Inhibitor Entinostat/Syndax 275 in Osteosarcoma.

Authors:  Simin Kiany; Douglas Harrison; Nancy Gordon
Journal:  Adv Exp Med Biol       Date:  2020       Impact factor: 2.622

9.  Clinical significance of nuclear factor (NF)-kappaB levels in urothelial carcinoma of the urinary bladder.

Authors:  Georgia Levidou; Angelica A Saetta; Penelope Korkolopoulou; Polyanthi Papanastasiou; Katerina Gioti; Petros Pavlopoulos; Kalliopi Diamantopoulou; Eupthemia Thomas-Tsagli; Konstantinos Xiromeritis; Efstratios Patsouris
Journal:  Virchows Arch       Date:  2008-03       Impact factor: 4.064

Review 10.  FLIP as an anti-cancer therapeutic target.

Authors:  Jin Kuk Yang
Journal:  Yonsei Med J       Date:  2008-02-29       Impact factor: 2.759

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