ABSTRACT
Objective To investigate the inhibitory effects of high mobility group chromosomal protein N2 (HMGN2)on growth of human bladder cancer T24 cells and ectopic tumor growth of nude mice. Methods MTT and flow cytometry assay were conducted to detect cell growth of bladder epithelial cells(T24)cells in vitro. The transplantation tumor models in nude mice were constructed by injecting T24 cells in vivo. The para-tumorswere injected with PBS,HMGN2 protein and cisdichlorodiamineplatinum(DDP),respectively. Tumor volume and weight were calculated. The expression of cell proliferation-related proteins was detected by Western blot assay. Results MTT assay proved that HMGN2 could significantly inhibit the growth of T24 cells. Flow cytometry assay verified that HMGN2 could block T24 cells in S stage of the cell cycle. The average tumor volume and weight in the HMGN2 group and DDP positive control group were smaller than those in the PBS group(P<0.05,respectively), with the tumor inhibitory rate of 25% and 23%,respectively. The results of Westernblot showed that HMGN2 could decrease Bcl-2 expression and increase Bax expression in tumor. Conclusion HMGN2 has a significant antitumor effect on T24 cells and bladder carcinoma in nude mice,which may be associated with the induction of the apoptosis of carcinoma cells and the regulation of the cell cycle.
ABSTRACT
High mobility group chromosomal protein B1 (HMGB1) and N2 (HMGN2), two members of High mobility group (HMG) family, play important role in inflammation. The purposes of this study were to investigate the expression of HMGB1 and HMGN2 in periodontistis. The expression of HMGB1 and HMGN2 mRNA in gingival tissues and gingival crevicular fluid (GCF) in chronic periodontitis (CP), generalized aggressive periodontitis (G-AgP) patients and healthy subjects was detected by real-time PCR. The protein level of HMGB1 and HMGN2 in peri-implant crevicular fluid (PICF), peri-implant crevicular fluid of peri-implantitis (PI-PICF) and normal patients was determined by Western blotting. Furthermore, IL-1â, IL-6, IL-8, TNF-á and HMGB1 levels in GCF, PI-PICF and healthy-PICF samples from different groups were determined by ELISA. HMGN2 expression was increased in inflamed gingival tissues and GCF from CP and G-ApG groups compared to control group. HMGB1 expression was the highest in the gingival tissues and GCF from CP patients and was accompanied by increased concentrations of IL-1â, IL-6, IL-8 proinflammaory cytokines. To our knowledge, this is the first study reporting that the expression of HMGB1 and HMGN2 was increased in the gingival tissues and GCF in CP and G-AgP and the PICF in PICF. Our data suggest that HMGB1 may be a potential target for the therapy of periodontitis and PI.