BioProject

The emergence of research on intratumoral bacteria and its correlation with the post-metastatic niche has garnered interest, yet the impact on liver metastasis of colorectal cancer through neutrophils remains unexplored. More...

The emergence of research on intratumoral bacteria and its correlation with the post-metastatic niche has garnered interest, yet the impact on liver metastasis of colorectal cancer through neutrophils remains unexplored. Our study confirmed the enrichment of ampicillin-resistant Escherichia coli (Am-R-E.coli) in the niche post-liver metastasis, revealing that Am-R-E.coli bolstered the release of neutrophil extracellular trap (NETs). This activation induced heightened expression of S100A8/9-STAT3 in colorectal cancer cells, resulting in increased invasion, migration, and proliferation. However, the precise mechanism remains unclear. Our recent findings indicated that RIPK2 enhanced the expression of ATF3/RelB in neutrophils and S100A8/9 interacted with STAT3 in tumor cells. As a result, we hypothesized that ATF3/RelB binds to the promoters of specific genes in neutrophils, leading to NETs release. Additionally, in tumor cells, S100A8/9 binding to STAT3 facilitated the proximity of promoters and enhancers of downstream genes through the common motifs. This study offered a theoretical foundation supporting the assertion that "intratumoral bacteria facilitate the liver metastasis of colorectal cancer," and contributed to the advancement of immunotherapy medications designed to target Am-R-E.coli and RIPK2. Less...