Effects of Spinach Powder Fat-Soluble Extract on Proliferation of Human Gastric Adenocarcinoma Cells

Four kinds of assays were used to study the effect of a fat-soluble extract of spinach powder (SPFE) on the proliferation of human gastric adenocareinoma cell line (SGC-7901) in vitro.These studies included: (Ⅰ) cell growth assay, (Ⅱ) colony forming assay, (Ⅲ) MTT colorimetric assay, and (Ⅳ) 3H-TdR incorporation assay. The concentrations of SPFE expressed as the level of β-carotene in the medium were 2×10-8, 2×10-7 and 2×10-6 mol/L β-carotene in assays (Ⅰ)～(Ⅲ), but 4×10- 8, 4×10-7 and 4×10-6 mol/L β-caretene in assay (Ⅳ) respectively. The results indicated that SPFE inhibited the prolifendion and colony forming ability of SGC-7901 cells. And in MTT assay, SPFE inhibited the viability of SGC7901 cells, but no inhibitory effect of SPFE was observed on the viability of lymphocytes in peripheral blood of healthy people. Finally, in the 3H-TdR incorporation test, both SPFE and β-carotene showed significant inhibitory effects on DNA synthesis in SGC-7901 cells, but SPFE was more effective than β-carotene.

CHEMOSENSITIVITY OF MGc80-3 HUMAN GASTRIC ADENOCARCINOMA CELLS AND ITS CLINICAL SIGNIFICANCE

In the present study, the chemosensitivity of MGc80-3 human gastric adenocarcinoma cells was determined by means of colony-forming assay and the in vitro activities of 10 anticancer drugs were examined on the basis of the clinically achievable peak plasma drug concentration. The results showed that MGc80-3 cells were most sensitive to mitomyc'n C, adriamycin and 5-fluorouracil, being consistent with the response noted in clinical gastric cancer. This cell line may retain its original drug sensitivity and may be useful in screening for new compounds with activity against this disease.

CLONING AND IDENTIFICATION OF A GENE RELATED TO THE DIFFERENTIATION OF HUMAN GASTRIC ADENOCARCINOMA CELLS

Objective: To compare the differential expression of mRNA between MKN-28 (highly differentiated) and MKN-45 (poorly differentiated) gastric adenocarcinoma cells and identify genes involved in human gastric adenocarcinoma differentiation. Methods: Differential expression of mRNA between MKN-28 and MKN-45 adenocarcinoma cells was investigated by fluorescent differential display (FDD). Differentially expressed cDNA was analyzed by bioinformatics and confirmed by RT-PCR and Northern-blot. Results: 45 differential fragments were finally attained. One of them (No. 10) was an approximate 750 bp cDNA and highly up-regulated in MKN-45 cells as compared with MKN-28 cells. By using Blastn and UniGene database analysis, we found the fragment was mapped to chromosome 14q11.2–q12 and showed a significant homology to Bcl-2 binding protein gene (BNip3), which was recently identified encoding pro-apoptosis protein located in mitochondrial. Conclusion: The BNip3 induced apoptosis could be suppressed by interacting with bcl-2. The BNip3 gene in tumor cells might be up-regulated by the hypoxia response element through the HIF1a transcription factor, causing death of the hypoxic cells at the center of the tumor where vascularization is usually poor in the process of tumor development.

Polymorphisms in tumor necrosis factor genes and susceptibility to esophageal squamous cell carcinoma and gastric cardiac adenocarcinoma in a population of high incidence region of North China

Background We investigated the possible association of the functional polymorphisms in the tumor necrosis factor （TNF） genes with susceptibility to esophageal squamous cell carcinoma （ESCC） and gastric cardiac adenocarcinoma （GCA）.Methods The TNF-α-308G/A and TNF-β ＋ 252G/A single nucleotide polymorphisms （SNPs） were genotyped using polymerase-chain reaction-restriction fragment length polymorphism （PCR-RFLP） analysis, in 555 cancer patients （291 ESCC and 264 GCA） and 437 healthy controls in a high incidence region of North China. Results Among healthy controls, frequencies of the TNF-α 1/1, 1/2 and 2/2 genotypes were 89.4% ,9.2% and 1.4% respectively, while frequencies of the TNF-β B1/B1, B1/B2 and B2/B2 genotypes were 12.6% , 32.3% and 55.1%, respectively. No significant difference was found in the overall genotype and allelotype distribution of the TNF-α-308G/A and TNF-β ＋ 252G/A SNPs among cancer patients and controls. However, both the B1/B1 genotype and B1/B2 genotype significantly increased the risk of developing ESCC [ the age and gender adjusted odds ratio （OR） =2.04 and 1.91, 95% confidence interval （CI） = 1.04 -4.43 and 1.14 - 2.60, respectively] and GCA （the age and gender adjusted OR =2. 68 and 2. 64, 95% CI = 1.14 -6.29 and 1.47 -4.72, respectively） in individuals with negative family history of UGIC, in comparison with the B2/B2 genotype. When the two TNF polymorphisms were combined and analyzed, individuals with the TNF-β B1/B2 and TNF-α1/2 or 2/2 genotypes significantly reduced the risk of developing ESCC and GCA, in comparison with those harboring the TNF-β B2/B2 and TNF-α 1/1 genotypes （ the age and gender adjusted OR = 0.37 and 0. 34, 95% CI =0. 15 -0.92 and 0. 13 -0.90, respectively）. Conclusions Therefore, the TNF-α -308G/A and TNF-β ＋ 252G/A genotyping may be used as a stratification markers to predicate the risk of ESCC and GCA development in North China.