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Shatha F Dallo1, Tao Weitao

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Anticancer drugs trigger bacterial evolution, enabling bacteria to invade cancer cells and evade treatment. This research reveals how bacteria develop these advantageous anti-cancer traits.

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Area of Science:

  • Microbiology
  • Cancer Biology
  • Drug Discovery

Background:

  • Anticancer drugs, specifically DNA replication inhibitors, can stimulate bacterial adhesion and induce the SOS response.
  • The SOS response in bacteria allows for the generation of mutants, potentially leading to the selection of novel phenotypes under drug pressure.

Purpose of the Study:

  • To test the hypothesis that bacteria evolve advantageous phenotypes to invade cancer cells and evade anticancer drugs.
  • To investigate if the SOS response, induced by anticancer drugs, facilitates the evolution of bacterial proteins mediating cancer cell capture and invasion.

Main Methods:

  • Examining the attachment and invasion of Pseudomonas aeruginosa and its SOS mutant to cancer cells in the presence of DNA replication inhibitors.
  • Identifying bacterial proteins with altered expression and the genes responsible for cancer adhesion and invasion.
  • Constructing gene mutants, cloning, and expressing identified genes to assess their role in bacterial interaction with cancer cells.

Main Results:

  • Differential induction of bacterial proteins during bacteria-cancer cell interaction under SOS response to anticancer drugs.
  • Disruption of bacterial adhesion and invasion phenotypes upon knockout of identified cancer-adhesion-invasion genes.
  • Confirmation that expression of these genes directs bacterial capture and invasion of cancer cells.

Conclusions:

  • Bacteria can evolve anti-cancer phenotypes targeting metastatic cells.
  • This evolutionary capability suggests potential for developing novel bacterial anti-metastasis therapeutic strategies.