Australian scientists know that, when it comes to prostate cancer, not all plasticity is good plasticity.
So a team led by Flinders University has been looking into how some prostate cancer cells can “switch” character so as to evade chemotherapy drugs, and they’ve identified a mechanism that causes the cells to sneakily evolve.
The findings are an important development in unravelling how an aggressive subtype of prostate cancer, neuroendocrine prostate cancer (NEPC), develops after hormonal therapies.
The lead researcher, Associate Professor Luke Selth from the Flinders Health and Medical Research Institute, said it is well established that some tumours show increased cellular “plasticity” in response to new or stressful conditions, such as cancer therapy.
“Increased cellular plasticity is increasingly recognised as a key feature by which prostate cancers become resistant to therapy and progress to a lethal stage,” Professor Selth said.
“Our new study reveals that a particular molecule, the microRNA ‘miR-194’, can enhance this plasticity in prostate cancer, leading to the emergence of NEPC.”
“By targeting miR-194, we were able to slow down and inhibit the growth of prostate cancer models with neuroendocrine features.”
Associate Professor Selth says while this study is a long way from clinical application, it: “nevertheless provides us with important new insights into how prostate cancers ‘evolve’ in response to therapy”.
Don’t be politically pliant and support our universities as they work to save lives – sign the petition to Keep It Clever now.