title: Role of FBXL20 in human colorectal adenocarcinoma.
abstract: In the present study, in order to determine whether the FBXL20 gene plays             a role in the carcinogenesis of human colorectal adenocarcinoma, the mRNA expression             levels of FBXL20 were examined in 30 pairs of human colorectal adenocarcinoma             tissues and corresponding adjacent normal colorectal tissues by quantitative real-time             PCR (qRT-PCR). The pGPU/GFP/Neo-FBXL20 siRNA expression vector was transfected             into the human colon carcinoma cell lines, SW480 and SW620. The mRNA levels of             β-catenin, c-Myc, cyclin D1, p53, PP2A, SET and E-cadherin were determined by             qRT-PCR, whereas the protein levels of β-catenin, c-Myc, caspase-3 and SET were             examined by western blot analysis. MTT assay and flow cytometry were employed             to assess cell proliferation, apoptosis and the cell cycle. As shown by qRT-PCR,             FBXL20 mRNA expression was upregulated in 76.7% of the tumor samples. Cell proliferation             was inhibited by 33.3% in the SW480-FBXL20 cells and by 22.7% in the SW620-FBXL20             cells, compared to the corresponding control cells. Furthermore, the percentages             of apoptotic cells were 21.3 and 17.1% in the SW480-FBXL20 and SW620-FBXL20 cells,             whereas the percentages of G1 phase cells in the two cell lines were 90.13 and             78.13%, respectively. In addition, the mRNA expression of SET and E-cadherin was             upregulated in the SW480-FBXL20 and SW620-FBXL20 cells, whereas that of β-catenin,             c-Myc, cyclin D1, p53 and PP2A was downregulated. Consistently, the protein expression             of β-catenin and c-Myc was downregulated, whereas that of SET and caspase-3 was             upregulated. Based on these results, we can conclude that FBXL20 plays an essential             role in the carcinogenesis of human colorectal adenocarcinoma. Moreover, our data             suggest that FBXL20 promotes carcinogenesis through the regulation of the Wnt             signaling pathway and caspase activation.
authors.affiliation: Department of Anatomy, Premedical and Forensic Medical Institute, Sichuan University, Chengdu, Sichuan 610041, PR China.
authors.forename: Jianjun
authors.initials: J
authors.lastname: Zhu
authors.forename: Kai
authors.initials: K
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Dong
authors.forename: Yao
authors.initials: Y
authors.lastname: Chen
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism*; D002453:Cell Cycle; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D015179:Colorectal Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D044783:F-Box Proteins / Q000235:genetics / Q000378:metabolism*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008297:Male; D008875:Middle Aged; D034622:RNA Interference; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering; D015398:Signal Transduction; D060449:Wnt Signaling Pathway
chemical_list: D016207:Cytokines; D044783:F-Box Proteins; C579745:FBXL20 protein, human; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D053148:Caspase 3