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Published on: July 6, 2013
Bacteria under SOS evolve anticancer phenotypes
1Biology Department, the University of Texas at San Antonio, One UTSA Circle, San Antonio, Texas 78249-0662, USA. tao.wei@utsa.edu.
Background:
The anticancer drugs, such as DNA replication inhibitors, stimulate bacterial adhesion and induce the bacterial SOS response. As a variety of bacterial mutants can be generated during SOS, novel phenotypes are likely to be selected under the drug pressure.
Presentation Of The Hypothesis:
Bacteria growing with cancer cells in the presence of the replication inhibitors undergo the SOS response and evolve advantageous phenotypes for the bacteria to invade the cancer cells in order to evade the drug attack. This hypothesis predicts that bacteria produce the proteins that mediate bacterial capture and invasion of cancer cells--the advantageous phenotypes. Generation of the phenotypes may be facilitated during the SOS response induced by anticancer drugs.
Experimental Design:
1) Examine attachment and invasion of bacterium Pseudomonas aeruginosa and the SOS mutant control to cancer cells in the presence of the anticancer drugs that inhibit DNA replication enzymes and trigger the SOS response. 2) Reveal the bacterial proteins that exhibit changes in expression. 3) Identify the genes encoding cancer adhesion and invasion. 4) Construct the mutants for the genes, clone and express these genes. 5) Examine the bacterial capture and invasion of cancer cells in contrast to non-cancer control.
Expected Results:
1) The bacterial proteins will be differentially induced during bacteria-cancer interaction under the SOS response to the anticancer drugs. 2) Knocking out the bacterial cancer-adhesion-invasion genes will disrupt the adhesion-invasion phenotypes of the bacteria. 3) Expressing these genes will direct the bacterial capture and invasion of cancer cells.
Implications Of The Hypothesis:
Bacteria can evolve anticancer phenotypes targeting metastatic cells. If this hypothesis is true, the outcomes will contribute to development of a novel bacterial anti-metastasis regimen.
Insights
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.
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.
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