Expressions and correlation analysis of HIF-1α, survivin and VEGF in patients with hepatocarcinoma.

OBJECTIVE: To investigate the expressions of HIF-1α, surviving, and VEGF in patients with hepatocarcinoma as well as the correlation analysis among them. PATIENTS AND METHODS: 65 patients, who were admitted to our hospital and diagnosed as hepatocarcinoma from January 2014 to October 2015, were selected as hepatocarcinoma group, while 50 healthy cases that do not have hepatocarcinoma were selected as normal control group. The expression levels of HIF-1α, surviving, and VEGF in hepatocarcinoma tissues of hepatocarcinoma group and normal liver tissues of control group were detected by immunohistochemical (SP) staining method; then, the correlation among them was explored. The expression levels of HIF-1α, surviving, and VEGF protein in hepatocarcinoma tissues and corresponding normal tissues were detected by Western blot. RESULTS: The positive expression rate of HIF-1α, surviving, and VEGF in hepatocarcinoma tissues of hepatocarcinoma group was respectively 46.2%, 55.4%, and 61.5%, significantly higher than that in cancer adjacent normal liver tissues of control group which was 2%, 2%, and 2%, and the differences were statistically significant (p<0.05). The expressions of HIF-1α, surviving, and VEGF in hepatocarcinoma tissues of patients with hepatocarcinoma were correlated with clinical stage, tumor differentiation degree and extrahepatic metastasis (p<0.05), but were not related to gender and tumor size (p>0.05). By Spearman rank correlation analysis, it could be seen that HIF-1α expression was positively correlated with VEGF protein expression in hepatocarcinoma tissues (r=0.683, p<0.05). Survivin expression was positively correlated with VEGF protein expression (r=0.717, p<0.05). There was no significant correlation between HIF-1α expression and survivin expression (p>0.05). The relative quantitative value of HIF-1α, surviving, and VEGF in hepatocarcinoma tissues of hepatocarcinoma group was respectively 3.04±0.23, 2.26±0.31, and 2.57±0.36, significantly higher than that in cancer adjacent liver tissues of control group which was 1.07±0.17, 1.31±0.27, and 1.42±0.43, and the differences were statistically significant (p<0.05). From Western blot electrophoresis scanning, it could be seen that the expressions of HIF-1α, surviving, and VEGF in hepatocarcinoma tissues were higher than those in cancer adjacent normal liver tissues. CONCLUSIONS: The expressions of HIF-1α, surviving, and VEGF played important roles in the occurrence, invasion, and metastasis of hepatocarcinoma. In hepatocarcinoma tissues, HIF-1α, and survivin protein expression was positively correlated with VEGF expression, but survivin protein was not related to HIF-1α expression, which indicated that HIF-1α and survivin may inhibit the apoptosis of hepatocarcinoma cells and promote tumor angiogenesis by up-regulating the expression of VEGF protein, thus accelerating the occurrence and development of hepatocarcinoma.

Association of gastric cancer with tyrosine hydroxylase gene polymorphism in a northwestern Chinese population.

Gastric cancer (GC) is a common and complex disease caused by multifactors. The aim of our study was to investigate the association of the common polymorphisms detected in insulin-like growth factor (IGF)-II, IGF-1 receptor, insulin-like growth factor binding protein 1 (IGFBP1), insulin (INS) and tyrosine hydroxylase (TH) with susceptibility to GC in a northwestern Chinese population. One hundred and fifty-four GC patients and 166 healthy controls were investigated in our study. The genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. The frequencies of CC and CT genotypes of TH were significantly higher in GC patients than in controls, as the odds ratios were 3.03 (95%CI 1.438-6.362, P=0.003) and 1.97 (95%CI 1.218-3.167, P=0.005), respectively. No association was found between the polymorphisms of IGF-II ApaI, insulin-like growth factor-1 receptor MnlI, IGFBP1 Bgl II and INS-23HphI and the development of GC. The presence of CC and CT genotypes of TH was associated with a significantly increased risk of GC. But the polymorphisms of other genes detected did not indicate an increased risk of GC in the investigated population.

The anti-proliferative effects of recombinant human lysozyme on human gastric cancer cells.

We investigated the anti-proliferative effects of recombinant human lysozyme (rHlys) on gastric cancer cell lines and normal human lung fibroblasts. Using conventional molecular cloning techniques we purified rHlys, which we incubated with cultured cells and measured the effects on cell proliferation and viability. At concentrations of 100 and 1000 microg/l, rHlys significantly inhibited the growth of human gastric cancer cell lines. In contrast, 10 and 50 microg/l of rHlys stimulated gastric cancer cell growth. None of the concentrations of rHlys affected cell viability. Only the highest concentration of rHlys (1000 microg/l) inhibited human lung fibroblast growth. Our results suggest that 100 microg/l is the optimum growth inhibiting concentration, which inhibited cancer cell growth but not normal cell growth. Our in vitro findings suggest that genetically engineered rHlys might inhibit human gastric cancer cell proliferation in vivo, so it might warrant further investigation as a potential novel anti-cancer agent.