RÉSUMÉ
Objective To explore the expression of HCCR, pERK and pELK1 in gastric cancer tissue and para-carci-noma tissue, and to explove its correlations. Methods In 60 human gastric cancers and their corresponding paraneo-plastic tissuses,the expression of HCCR, pERK and pELK1 were detected by immunohistochemistry. Results The ex-pression of HCCR was 75.0%(45/60), pERK, and pELK1 were 73.3%(44/60) and 71.7%(43/60), respectively, and the expression of proteins in gastric tumor were higher than that in paraneoplastic tissues (P<0.05). Conclusion The HCCR, pERK and pELK1 are higher expressed in tumor tissues, availably as a auxiliary index for clinical immunohis-tochemistry in gastric cancer.
RÉSUMÉ
Objective To investigate the effects of antisense recombinant euraryotic expression vector of HCCR-2 on the proliferation and apoptosis of HepG2. Methods The antisense recombinant eukaryotic expression vector of HCCR-2 was constructed. The vector was stably transfected to the HepG2 cells, and positive clones were selected by G418 (antiseuse vector group), pIRES2-EGFP vector was transfected into the HepG2 cells in the same way (pIRES2-EGFP group). The conditions of the nontransfected HepG2 cells were used as control (HepG2 group). Changes in cell growth curve, cell cycle, cell apoptosis and morphology of HepG2 cells after the transfec-tion were detected by MTT method, flow cytometry and transmission electron microscopy, respectively. All the data were analyzed by one-way ANOVA and chi-square test. Results The expression level of HCCR-2 mRNA was down-regulated to 0.39±0.04 in antisense vector group, and the expression level of HCCR-2 mRNA in pIRES2-EGFP group and HepG2 group were 0.62±0.06 and 0.72±0.03, respectively, with significant difference among the 3 groups (F=43.701, P<0.05). The apoptotic rate of HepG2 cells in antisense vector group, pIRES2-EGFP grop and HepG2 group were 13.30%, 2.51% and 2.07%, respectively, with significant difference among the 3 group (χ2=6.793, 8.721, P<0.05). The growth of HepG2 cells in antisense vector group was retarded, and was blocked in G0/G1 stage. Conclusions The HCCR-2 antisense recombinant eukaryotic expression vector can inhibit the mRNA expression of HCCR-2 and promote the apoptosis of cells. HCCR-2 may be involved in cell regulation and the proliferation of hepatocellular carcinoma cells.