Quantitative evaluation of transcriptional activation of NF-κB p65 and p50 subunits and IκBα encoding genes in colon cancer cells by Desulfovibrio desulfuricans endotoxin

Abstract

Quantification of p65, p50 and IκBα mRNAs was performed by real time QRT-PCR in Caco-2 cells treated with 10, 50, and 100 μg/mL of Desulfovibrio desulfuricans LPS for 1, 6, 12, and 24 h. A strong increase in expression of p65 and IλBα genes was induced by 10 and 100 μg/mL of LPS at 1 h; after 6 h higher transcript amounts of both genes were observed at 100 μg/mL LPS. The p65 expression level was significantly increased by 50 and 100 μg/mL at 12 h and lowered by all LPS doses at 24 h. No significant differences between IκBα mRNA quantity in cells exposed to LPS at 12 and 24 h were observed. No changes in expression of p50 mRNA were induced by LPS. The expression of p65 gene positively correlated with IκBα gene expression. D. desulfuricans LPS is capable of modulating transcriptional activity of p65 and IκBα genes in intestinal epithelial cells.

Foes or Friends? Bacteria Enriched in the Tumor Microenvironment of Colorectal Cancer

“…These studies may explain the role of Desulfovibrio in cancer development. Besides, the LPS of D. desulfuricans is capable of modulating transcriptional activity of NF-κB, p65, and IκBα encoding genes in colon cancer cells [90]. Although there is no direct evidence that Desulfovibrio can cause CRC, Desulfovibrio is possibly playing a role in the development of CRC.…”

<p>Analyses of Potential Driver and Passenger Bacteria in Human Colorectal Cancer</p>

“…4 Candidate driver bacteria show procarcinogenic features such as production of DNAdamaging compounds, interruption of tumor suppressor protein function, and induction of host inflammatory response. 5,6 These bacteria may colonize with low relative abundance but persistently interact with host cells to induce asymptomatic but chronic change in normal intestinal epithelium to initiate CRC. 7 Candidate passenger bacteria may show low relative abundances at the normal intestinal epithelium or the early stage of CRC, but competitively proliferate in the latter tumor niche.…”

Expression of the inflammatory regulator A20 correlates with lung function in patients with cystic fibrosis

“…LPS induces A20, which in turn inhibits NF-κB activity. LPS selectively increases the transcriptional activity of p65, but not p50, in intestinal epithelial cells [15]. In line with this, overexpression of p65 increases NF-κB transcriptional activity [16].…”