Overexpression of the Survivin gene in SGC7901 cell resistance to cisplatin.

The aim of the present study was to investigate the mechanism of SGC7901 cell resistance to cisplatin (CDDP). SGC7901/CDDP cells were established by the long-term continuous exposure of SGC7901 cells to CDDP in stepwise concentration increments. The morphologies of the SGC7901/CDDP and SGC7901 cells were observed by microscopy. The expression levels of Survivin mRNA and protein in the SGC7901/CDDP and SGC7901 cells were examined by reverse transcription polymerase chain reaction and western blotting respectively. The results revealed morphological differences between the SGC7901 and SGC7901/CDDP cells. The expression levels of Survivin mRNA and protein were significantly higher in the SGC7901/CDDP cells than in the SGC7901 cells. Therefore, high expression levels of the Survivin gene may explain SGC7901 cell resistance to CDDP.

The effects of aspirin plus cisplatin on SGC7901/CDDP cells in vitro.

The purpose of this study was to determine the effect of aspirin plus cisplatin (CDDP) in the chemotherapy of gastric cancer. We cultured SGC7901/CDDP cells by long-term exposure of SGC7901 cells to small doses of CDDP in vitro. The cells were treated with aspirin, CDDP or aspirin plus CDDP for 24 h and cell growth was assessed by the MTT assay, the apoptotic rate by flow cytometry, the survivin mRNA expression by RT-PCR and the survivin protein expression by western blotting. The results revealed that the cell growth in the aspirin plus CDDP group was significantly inhibited. The apoptotic rate in the aspirin plus CDDP was significantly higher compared to that in the other groups. The survivin mRNA and protein expression were also significantly reduced in the aspirin plus CDDP group. Our data suggest that the combination of aspirin and CDDP exhibited a higher degree of toxicity against SGC7901/CDDP cells compared to that of aspirin or CDDP alone. Thus, the combination of aspirin plus CDDP may reduce the expression of survivin and induce the apoptosis of SGC7901/CDDP cells.

[Expression and clinical significance of secretory leucocyte protease inhibitor in colon carcinoma].

OBJECTIVE: To investigate the expression of secretory leucocyte protease inhibitor (SLPI) in colon cancer and their clinical significance. METHODS: Immunohistochemistry was performed to detect the SLPI expression in colon cancer tissue microarray. The expression of SLPI was scored by two pathologists and was analyzed using Χ(2) test to explore its influence on the pathologic characteristics of colon carcinoma. RESULTS: SLPI was up-regulated in colon cancer tissue compared to normal mucosa. Overexpression of SLPI protein was correlated with differentiation grade (low differentiation: 42.1% vs 57.9%; moderate/well differentiation: 2.3% vs 97.7%, TNM stages(III-IV:29.4% vs 70.6%;I-II:3.1% vs 96.9%), lymph node metastasis (28.6% vs 71.4%) and distant metastasis (84.6% vs 15.4%), but not with patient age or sex. CONCLUSION: SLPI overexpression correlates with aggressive pathologic characteristics of colon cancer and it may server as prognostic factor of colon cancer patients. Further research will be carried out to verify whether SLPI can become a new target for colon cancer treatment.

[Application of genome-wide microarray for screening genes related to peritoneal metastasis of colorectal cancer].

OBJECTIVE: To screen genes related to peritoneal metastasis of colorectal cancer. METHODS: Specimens of primary cancer and normal mucosa tissues were collected from 3 patients with peritoneal metastasis of colorectal cancer. The total RNA were extracted and inversely transcribed into cDNA to synthesize aRNA using in vitro RNA synthesis. The synthesized aRNA, after labeling with Cy3, were hybridized with the whole human genome oligo microarray. The Empirical Bayes method was used to screen the differentially expressed genes, followed by confirmation of the selected genes by semi-quantitative RT-PCR. RESULTS: With a threshold of P≤0.05, a total of 105 differentially expressed genes were identified in primary cancer lesions, including 42 up-regulated and 63 down-regulated genes. Three of the up-regulated genes (S100P, PRDX1 and SLPI) were selected and confirmed by RT-PCR, which yielded results consistent with those from gene microarray. CONCLUSION: Gene microarray technique can provide valuable clues for locating the tumor markers of peritoneal metastasis in colorectal cancer patients.