URG4/URGCP ENHANCES THE ANGIOGENIC CAPACITY OF HUMAN HEPATOCELLULAR CARCINOMA CELLS IN VITRO VIA ACTIVATION OF THE NF-ΚB SIGNALING PATHWAY

Angiogenesis is essential for tumor growth. Hepatocellular carcinoma (HCC) is characterized by hypervascularity; high levels of angiogenesis are associated with poor prognosis and a highly invasive phenotype in HCC. Up-regulated gene-4 (URG4), also known as upregulator of cell proliferation (URGCP),[r]

protein IjB [5,6]. NF-jB is activated by various stim-uli, including tumor necrosis factor (TNF), interleukin-1(IL-1) and lipopolysaccharide (LPS) [7,8]. It is thentransported to the nucleus, where it binds to specificsequences in the promoter or enhancer region of targetg[r]

was also insensitive to the inhibitor, as well as to coexpres-sion of inhibitory mutants of the p38 and MK2 kinases(Fig. 2). Insensitivity of UV-induced stabilization to each ofthe two mutants alone would have left the possibility thatp38 MAP kinase activate[r]

SUMOylation, an important post-translational modification, associates with the development of hepatocellular carcinoma (HCC). p65, one of the most important subunits of NF-κB, is a key regulator in the development of HCC and has been reported to be SUMOylated by exogenous small ubiquitin-related mod[r]

The activation of TLR3 was associated with malignant progression and prognosis of patients. HCC is the sec- ond most frequent cause of cancer death. Because of the development of improved treatment strategies and mon- itoring methods,