AIM： To detect the expression of a proliferation-related ligand on human hepatocellular carcinoma （HCC） cell lines （SK-Hepl, HLE and HepG2） and in culture medium. METHODS： APRIL expression was analyzed by Wester...AIM： To detect the expression of a proliferation-related ligand on human hepatocellular carcinoma （HCC） cell lines （SK-Hepl, HLE and HepG2） and in culture medium. METHODS： APRIL expression was analyzed by Western blotting in HCC cell lines. Effects of APRIL to cell count and angiogenesis were analyzed, too. RESULTS： Recombinant human APRIL （rhAPRIL） increased cell viability of HepG2 cells and, in HUVEC, rhAPRIL provided slight tolerance to cell death from serum starvation. Soluble APRIL （sAPRIL） from HLE cells increased after serum starvation, but did not change in SK-Hepl or HepG2 cells. These cells showed down-regulation of VEGF after incubation with anti-APRIL antibody. Furthermore, culture medium from the HCC cells treated with anti-APRIL antibody treatment inhibited tube formation of HUVECs. CONCLUSION： Functional expression of APRIL might contribute to neovascularization via an upregulation of VEGF in HCC.展开更多
文摘AIM： To detect the expression of a proliferation-related ligand on human hepatocellular carcinoma （HCC） cell lines （SK-Hepl, HLE and HepG2） and in culture medium. METHODS： APRIL expression was analyzed by Western blotting in HCC cell lines. Effects of APRIL to cell count and angiogenesis were analyzed, too. RESULTS： Recombinant human APRIL （rhAPRIL） increased cell viability of HepG2 cells and, in HUVEC, rhAPRIL provided slight tolerance to cell death from serum starvation. Soluble APRIL （sAPRIL） from HLE cells increased after serum starvation, but did not change in SK-Hepl or HepG2 cells. These cells showed down-regulation of VEGF after incubation with anti-APRIL antibody. Furthermore, culture medium from the HCC cells treated with anti-APRIL antibody treatment inhibited tube formation of HUVECs. CONCLUSION： Functional expression of APRIL might contribute to neovascularization via an upregulation of VEGF in HCC.
