Certain strains of E. coli bacteria produce a mutagenic genotoxin called colibactin, which is suspected of causing colorectal cancer. Researchers at the Max Planck Institute for Infection Biology in Berlin headed by Professor Dr. Thomas F. Meyer have now succeeded in directly observing the colibactin's mode of action directly in cells. For this purpose, they cultivated mucosal cell organoids from the colon derived from adult intestinal stem cells. The organoids
were exposed to colibactin-producing E. coli bacteria for three hours.

The scientists were able to observe that colibactin alters the host cell DNA in such a way that they behave like colon cancer cells. Normally, the organoid cells continuously require a certain growth factor (Wnt) to proliferate. Without this growth factor, the cells differentiate into specialized cells just as they do in the healthy intestine and die a short time later. However, the colibactin-influenced cells proliferate independently of the Wnt signal. This results in uncontrolled growth, a precursor to cancer.

DNA sequencing of the Wnt-independent organoids showed that the DNA had numerous mutations, including crude structural alterations in which entire sections of chromosomes had been restructured or lost. In particular, the genetic material for the tumor suppressor protein p53 was altered. It protects the cell from tumor development by arresting the cell cycle in the G1 phase during its mitosis or by or initiating cell death¹.

The researchers have published their work in the journal Nature Communications.
Iftekhar, A., Berger, H., Bouznad, N., Heuberger, J., Boccellato, F., Dobrindt, U., Hermeking, H., Sigal, M. & Meyer, T. F. (2021). Genomic aberrations after short-term exposure to colibactin-producing E. coli transform primary colon epithelial cells. Nature Communications.

Source:
https://www.mpg.de/16411957/0212-infe-auf-frischer-tat-ertappt-wie-bakterien-gesunde-zellen-in-krebszellen-umwandeln-152585-x

¹ https://www.spektrum.de/lexikon/biologie/p53-protein/53394