Search

The genome of lethal animal pathogenic bacterium Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is characterized by the presence of multiple pathogenicity islands (PAIs). Computational methods have been developed to identify PAIs based on the distinguishing G+C levels in some PAI versus non-PAI regions. We observed that PAIs can have a very similar G+C level to that of the host chromosome, which may have led to false negative predictions using these methods. We have applied a novel method of genomic barcodes to identify PAIs. Using this technique, we have successfully identified both known and novel PAIs in the genomes of three strains of EHEC O157:H7.

The present study reported that the ubiquitin ligase Cbl-b was up-regulated during anthracycline-induced apoptosis in two cell lines, RBL-2H3 leukemia cells and MGC803 gastric cancer cells. Overexpression of Cbl-b strongly promoted the cytotoxic and apoptosis-inducing effects of anthracyclines, while a dominant negative (DN) Cbl-b mutation abolished these effects in both cell lines. Further investigation revealed that mitochondrial depolarization was enhanced by Cbl-b and decreased by Cbl-b (DN) in RBL-2H3 cells. Moreover, overexpression of Cbl-b significantly suppressed ERK activation, and Cbl-b (DN) strongly enhanced both ERK and Akt activation. Altogether, these results indicate that Cbl-b sensitized both leukemia and gastric cancer cells to anthracyclines by activating the mitochondrial apoptotic pathway and modulating the ERK and Akt survival pathways.

We previously showed that high expression levels of SOX9 correlate with hepatocellular carcinoma (HCC) progression. However, the exact role that SOX9 plays in HCC remains unclear. In this study, we firstly confirmed that miRNA-101 directly targets SOX9 in HCC. Ectopic expression of miR-101 significantly inhibited HCC cell proliferation and tumorigenicity by targeting SOX9. Moreover, the down-regulation of miR-101 in clinical HCC tissues correlates with tumor aggressiveness and poor prognosis. Therefore, miR-101 may suppress HCC tumor progression by down-regulating SOX9. MiR-101 may be a potential prognostic marker and therapeutic target for HCC.