作者: Vanessa Andries , Karl Vandepoele , Katrien Staes , Geert Berx , Pieter Bogaert
DOI: 10.1186/S12885-015-1408-5
关键词: HEK 293 cells 、 Downregulation and upregulation 、 Cell cycle 、 Biology 、 Immunology 、 Cell culture 、 Carcinogenesis 、 G1 phase 、 Cancer research 、 NBPF1 、 Neuroblastoma
摘要: NBPF1 (Neuroblastoma Breakpoint Family, member 1) was originally identified in a neuroblastoma patient on the basis of its disruption by chromosomal translocation t(1;17)(p36.2;q11.2). Considering this genetic defect and frequent genomic alterations locus several cancer types, we hypothesized that is tumor suppressor. Decreased expression cell lines with loss 1p36 heterozygosity marked decrease anchorage-independent clonal growth DLD1 colorectal carcinoma cells induced further suggest functions as However, little known about mechanisms involved. Expression NBPF analyzed human skin cervix immunohistochemistry. The effects cycle were evaluated flow cytometry. We investigated real-time quantitative RT-PCR profile panel genes important regulation. Protein levels CDKN1A-encoded p21CIP1/WAF1 determined western blotting importance p53 shown immunofluorescence loss-of-function approach. LC-MS/MS analysis used to investigate proteome colon expression. Possible biological interactions between differentially regulated proteins Ingenuity Pathway Analysis tool. show expressed non-proliferative suprabasal layers squamous stratified epithelia cervix. Forced HEK293T resulted G1 arrest accompanied upregulation cyclin-dependent kinase inhibitor p53-dependent manner. Additionally, forced two p53-mutant also CDKN1A upregulation. not observed cells, which demonstrates exerts cell-specific effects. In addition, NBPF1-overexpressing 32 proteins, are implicated carcinogenesis. demonstrated different suppressive effects, depending line analyzed, provide new clues into molecular mechanism enigmatic proteins.