| Kasiappan R |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=4.533 ------>paper_class3=2 ------>paper_class2=1 ------>vol=7 ------>confirm_bywho=jschu ------>insert_bywho=jschu ------>Jurnal_Rank=24.8 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=548 ------>medlineContent= ------>unit=E0102 ------>insert_date=20091013 ------>iam=7 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Molecular Cancer Research ------>paper_name=Loss of p53 and MCT-1 overexpression synergistically promote chromosome instability and tumorigenicity ------>confirm_date=20091013 ------>tch_id=087008 ------>pmid=19372582 ------>page1=536 ------>fullAbstract=MCT-1 oncoprotein accelerates p53 degradation by means of the ubiquitin-dependent proteolysis. Our present data show that induction of MCT-1 increases chromosomal translocations and deregulated G(2)-M checkpoint in response to chemotherapeutic genotoxin. Remarkably, increases in chromosome copy number, multinucleation, and cytokinesis failure are also promoted while MCT-1 is induced in p53-deficient cells. In such a circumstance, the Ras-mitogen-activated protein kinase/extracellular signal-regulated kinase kinase-mitogen-activated protein kinase signaling activity and the expression of metastatic molecules are amplified. Given a p53-silencing background, MCT-1 malignantly transforms normal breast epithelial cells that are satisfactory for stimulating cell migration/adhesion and tumorigenesis. Detailed analyses of MCT-1 oncogenicity in H1299 p53-null lung cancer cells have shown that ectopically expressed MCT-1 advances xenograft tumorigenicity and angiogenesis, which cannot be completely suppressed by induction of p53. MCT-1 counteracts mutually with p53 at transcriptional levels. Clinical validations confirm that MCT-1 mRNA levels are differentially enriched in comparison between human lung cancer and nontumorigenic tissues. The levels of p53 mRNA are comparatively reduced in a subset of cancer specimens, which highly present MCT-1 mRNA. Our results indicate that synergistic promotions of chromosomal imbalances and oncogenic potency as a result of MCT-1 expression and p53 loss play important roles in tumor development. ------>tmu_sno=None ------>sno=22547 ------>authors2=Shih HJ ------>authors3=Chu KL ------>authors4=Chen WT ------>authors5=Liu HP ------>authors6=Huang SF, Choy CO, Shu CL, Din R, Chu JS, Hsu HL ------>authors6_c= ------>authors=Kasiappan R ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Loss of p53 and MCT-1 overexpression synergistically promote chromosome instability and tumorigenicity. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no=4 ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2009 ------>submit_flag=None ------>publish_month=4 |