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.
Over a period of 3 years' study (2012)(2013)(2014), a total of 518 faecal samples were collected and cultured to isolate Escherichia coli. Of these, 338 (65.3 %) E. coli isolates were recovered from infants, and 142/338 (42 %) were multidrug-resistant (MDR) to $3 drug classes using the antimicrobial susceptibility disc diffusion method. A total of 125/142 (88 %) of E. coli isolates were extended-spectrum b-lactamase (ESBL) producers. blaCTX-M-15 types were observed in 80/125 (64 %) of the isolates, and 60/80 (75 %) were positive for blaCTX-M-15. Out of 338 E. coli isolates, 9 (2.6 %) were positive for ST131/O25b clone and each isolate was associated with several plasmids of different sizes (1-21.2 kb). The identities of these nine isolates were confirmed by sequencing for presence of pabB (347 bp) and trpA (427 bp) genes. This study demonstrates low prevalence rate of the highly virulent E. coli ST131 clone producing blaCTX-M-15 in the intestines of Jordanian infants.
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