Saint Louis University  Inventor: Barrie P. Bode, Ph.D.   In
liver diseases including hepatocellular carcinoma (HCC) and
cirrhosis there is a net increase in glutamine consumption that
subverts the systemic glutamine homeostatic function of the
liver and results in reduced plasma glutamine levels that can
adversely impact the glutamine-dependent cells of the immune
system. HCC cells take up glutamine at rates 10 to 30-fold
faster than normal hepatocytes.  A cDNA has been isolated that
encodes for a broad specificity Na+-dependent glutamine
transporter referred to as "ATB0". The properties of ATB0 match
those reported for the System ASC-like hepatoma activity that is
reported to govern glutamine-dependent growth in SK-Hep human
hepatoma cells. Specific down-regulation of ATB0 activity in
hepatoma cells culminates in death of the hepatoma cells by
apoptosis.  Agents useful for inhibiting ATB0 activity include
antibodies against ATB0, siRNAs that target ATB0 RNA for
destruction, and, various ATB0 inhibitory smal