Hepatocellular carcinoma up-regulated long non-coding RNA (HULC)

Hepatocellular carcinoma up-regulated long non-coding RNA (HULC) is a long non-coding RNA (lncRNA) found on chromosome 6p24.3, with a transcript length of approximately 500 nucleotides[3][4]. HULC was first noted for its striking overexpression in hepatocellular carcinoma but is upregulated in a variety of cancers, including gastric, glioma, pancreatic, and ovarian carcinomas[1][2][3][7][8]. Functionally, HULC acts as an oncogene, promoting tumor cell proliferation, migration, invasion, and inhibiting apoptosis and autophagy, in part through regulation of proteins including ATG7, LC3, SQSTM1, and ITGB1[1]. Mechanistically, HULC modulates gene expression post-transcriptionally, serves as a microRNA sponge, and is implicated in epigenetic regulation[1][2][5][8]. Its expression level in plasma or tissues has strong prognostic relevance, correlating with tumor grade, hepatitis B status, and clinical outcome in liver and other cancers[2][3][8]. HULC’s multifaceted involvement in oncogenesis, metastasis, and tumor progression makes it both a promising biomarker and a potential therapeutic target, although clinical translation faces delivery and specificity hurdles for lncRNA-targeted therapies[1][2][8].

Other names

NCRNA00078LINC00078HCCAT1Non-protein coding RNA 78Long intergenic non-protein coding RNA 78Hepatocellular carcinoma associated transcript 1 (non-protein coding)LOC100506207Highly up-regulated in liver cancer (non-protein coding)Highly up-regulated in liver cancer long non-coding RNAHULC[5]

Drugs or interventions targeting HULC typically act via RNA interference (siRNA), modulation of autophagy-related proteins (e.g., ATG7), and modulation of epithelial–mesenchymal transition (EMT) and vasculogenic mimicry in tumors.