Mol Med 2002, 8: 725–32.PubMed 26. Galligan L, Longley DB, McEwan M, Wilson TR, McLaughlin K, Johnston PG: Chemotherapy and TRAIL-mediated colon cancer cell death: the roles of p53, TRAIL receptors, and c-FLIP. Mol Cancer Ther 2005, 4: 2026–36.CrossRefPubMed 27. Longley DB, Wilson TR, McEwan M, Allen WL, McDermott U, Galligan L, Johnston PG: c-FLIP inhibits chemotherapy-induced colorectal cancer cell death. Oncogene 2006, 25: 838–48.CrossRefPubMed Competing interests The authors declare that they selleck products have no competing interests. Authors’ contributions XD and GB participated in the preparation of the tissue sections and the construction of the siRNA vectors, and helped in coordinating

the work. GB also participated in data analysis and interpretation and in BI 10773 in vitro manuscript preparation. XH and QQ have been involved in western blot analysis, PCR assays and IHC and ICC assays of c-FLIP expression. HZ and FY participated

in cell culture and cellular work. JL participated in study design and critical revision of the manuscript. QM participated in the study design and coordination and helped to revise the manuscript. All authors read and approved the final manuscript.”
“Introduction A number of genes for apoptosis play an important role in tumorigenesis [1]. Several gene abnormalities were reported as prognostic Inhibitor Library price markers of non-small cell lung cancer, such as p53 [2]; however, these processes are complex and remain unclear. The abnormal expression of p53 is frequently reported in a variety of cancers [3]. p53 mutations are generally more common in Calpain smokers than in nonsmokers and an excess of G to T transversions of p53 has been described as a molecular signature of tobacco smoke mutagens in smoking-associated lung cancers. There are also mutational

hotspots (codons 157, 158, 245, 248, and 273) in the p53 gene in lung cancer [4]. Several reports have shown that p53 expression is a prognostic marker in non-small cell lung cancer [2]. p53 protein is a tumor suppressor gene and mediates cell cycle arrest or programmed cell death [5, 6]. These p53-mediated events were triggered through the transactivation of specific genes, including p21, GADD45, cyclin G1, Bax, and fas [7, 8]. Recently, we reported that p53AIP1, which is a new potential mediator of p53-dependent apoptosis, is associated with prognosis in non-small cell lung cancer [9]. p53AIP1 is not normally expressed in any tissues except the thymus, but is induced when Ser-46 of p53 was phosphorylated after severe DNA damage [10, 11]. Only a few papers have reported p53AIP1 function in cancer biology and it has not been well investigated [9, 12]. On the other hand, survivin is a member of the IAP gene family, which has been implicated in both the inhibition of apoptosis and mitosis regulation [13].