ABSTRACT
<p><b>OBJECTIVE</b>To investigate the taxonomic richness and diversity of gut microbiota in patients with colorectal adenoma and elucidate the role of gut microorganisms in precancerous lesions in the colon and rectum.</p><p><b>METHOD</b>Adenomatous tissues from 31 patients with colorectal adenoma and normal intestinal mucosal tissues from 20 healthy control subjects were collected through colonoscopy. The total bacterial genomic DNA was extracted, and the V-Vhypervariable region in bacterial 16S rRNA gene was amplified using polymerase chain reaction and sequenced on an Illumina MiSeq platform.</p><p><b>RESULTS</b>Patients with colorectal adenomas had a higher alpha diversity and richness indices compared to the healthy controls (P<0.01). The mucosal microbiota in colorectal adenoma tissue showed a distinctive structural difference from that in normal intestinal mucosal tissues. At the phylum level, a large decrease in Firmicutes with concomitant relative expansion of Proteobacteria was observed in patients with colorectal adenomas, resulting in a significant decrease in the Firmicutes/Bacteroidetes ratio (P<0.01). At the genus level, Lactococcus and Pseudomonas were enriched whereas Enterococcus, Bacillus, and Solibacillus were reduced obviously in the preneoplastic tissues (P<0.01). We also found a similar gut microbiome composition between low-grade and high-grade intraepithelial neoplasia; the ratio of Escherichia-Shigella tended to increase in high-grade intraepithelial neoplasia, but this change was not statistically significant (P%0.28).</p><p><b>CONCLUSION</b>Significant changes in the structure of the intestinal flora occur in patients with colorectal adenomas, indicating that the association of dysbiosis of the gut microbiota with the occurrence of a pro-oncogenic microenvironment.</p>
ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of nimesulide, a selective COX-2 inhibitor, on cell viability, telomerase and PKB activities in human gastric cancer cell line SGC7901 and to explore its molecular mechanism of selective growth inhibition.</p><p><b>METHODS</b>MTT assay was used to determine cell viability after incubation for 0, 12, 24, and 48 h in different concentrations (0, 25, 50, 100, 200 micro mol/L) of nimesulide and/or okadaic acid (300 nmol/L). Telomerase and protein kinase B (PKB) activities were detected using TRAP PCR-ELISA and nonradioactive IP-kinase assay.</p><p><b>RESULTS</b>Nimsulide caused a time and dose-dependent reduction of cell numbers of SGC7901. The telomerase and PKB activities were significantly inhibited, and the inhibition of telomerase activity was partly associated with decrease in PKB activity.</p><p><b>CONCLUSION</b>Selective COX-2 inhibitor nimesulide inhibits telomerase activity of gastric cancer cells by partly blocking the activation of protein kinase B. The results suggest an additional signaling pathway underlying the anti-cancer effect of COX-2 inhibitor.</p>