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HULC: Highly upregulated in liver cancer RNA
Competing endogenous RNA (ceRNA). Functions as a sponge/ target mimic for miR-372 through a conserved target site, reducing the expression and activity of miR-372 (Wang (2010)). One of targets of miR-372 is Prkacb (catalytic subunit of PKA) which is able to phophorylate CREB. Hence expression of HULC stimulates further HULC expression by inhibiting miR-372, and allowing PRKACB to create active CREB (Wang (2010)). HULC knockdown affects expression of other genes including some described in liver cancer (Panzitt (2007)).
Binding of phospho-CREB to the HULC promoter activates HULC expression. Phosphorylation of CREB was stimulated by PKA signaling (Wang (2010)). Highly up-regulated in hepatocellular carcinoma (HCC) and to a lesser extent in liver focal nodular hyperplasia (FNH). Up-regulation was specific to HCC with high expression not detected in normal liver, other tissues and their associated neoplasms (Panzitt (2007)). HULC expression was also up-regulated in colorectal carcinomas that metastasised to the liver but not in primary colorectal carcinomas or carcinomas that metastasised to lymph nodes (Matouk (2009)). HULC RNA could be detected in the blood of HCC patients (Panzitt (2007)). Localised to the cytoplasm, may associate with ribosomes, but no sign of translated products could be found (Panzitt (2007)). HULC expression was also identified in 3 old world monkeys (Panzitt (2007)).
HLUC also present in other primates, gene shows good conservation above that of surrounding sequence. Not detected in rodents so may be primate specific (Panzitt (2007)).
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Allelic Information and Variation
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