Basic & Clinical Medicine ›› 2018, Vol. 38 ›› Issue (10): 1417-1421.

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HMGB1 promotes cell proliferation of primary hepatocellular carcinoma


  • Received:2017-09-21 Revised:2018-01-25 Online:2018-10-05 Published:2018-09-28
  • Contact: Wen-Yu CAO

Abstract: Objective To investigate the expression of the high-mobility group box-B1 (HMGB1) and the receptor for advanced glycation endproduct (RAGE) in primary hepatocellular carcinoma, and to study the effect of HMGB1 on the proliferation of hepatocarcinoma cells and the related molecular mechanism. Methods 25 cases of hepatocellular carcinoma tissues and corresponding normal liver tissues were collected and the expression levels of HMGB1 and RAGE in the tissue samples were observed by immunohistochemistry. HepG2 cells and normal L02 hepatocytes were cultured in vitro, and Western blot was used to detect the expression of HMGB1 and RAGE. HepG2 cells was pretreated with recombinant human HMGB1 (rhHMGB1) at different concentrations (0, 10, 50 and 100 μg/L) and for different time (0, 12, 24 and 36 h), and then MTT assay were used to detect the proliferation of HepG2 cells. The expression of RAGE and NF-κB in HepG2 cells was detected by Western blot. Results The positive expression rates of HMGB1 and RAGE protein in hepatocellular carcinoma tissues were 64% and 72%, and much higher than corresponding normal liver tissues of 20% and 28% (P <0.05). With the prolongation of cell culture time, the expression of HMGB1 and RAGE increased. With the increase of rhHMGB1 concentration or the prolongation of treatment time, the proliferation rate of HepG2 cells was significantly increased (P <0.05), and the expression of RAGE and NF-κB was up-regulated (P <0.05). Conclusions HMGB1 and RAGE protein are highly expressed in hepatocellular carcinoma tissues and hepatocarcinoma cells. HMGB1 may activate NF-κB signaling pathway by binding to its receptor RAGE, thereby promoting the proliferation of hepatocellular carcinoma cells.

Key words: Primary Hepatocellular Carcinoma, HMGB1, RAGE, HepG2 cells, Cell proliferation