In a new study, researchers found a new mechanism in which prostate cancer cells can ‘switch’ character and become resistant to therapy.
These findings are an important development in unraveling how an aggressive subtype of prostate cancer, neuroendocrine prostate cancer (NEPC), develops after hormonal therapies.
The research was conducted by a team from the Flinders Health and Medical Research Institute.
It is well established that some tumors show increased cellular ‘plasticity’ in response to new or stressful conditions, such as cancer therapy.
This plasticity allows the cancer cells to adapt and continue to grow by evolving into different cell types that no longer respond to the therapy.
The team says increased cellular plasticity is increasingly recognized as a key feature by which prostate cancers become resistant to therapy and progress to a lethal stage.
The new study shows 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, the researchers were able to slow down and inhibit the growth of prostate cancer models with neuroendocrine features.
While this study is a long way from clinical application, it nevertheless provides doctors with important new insights into how prostate cancers ‘evolve’ in response to therapy.
There are currently no effective treatments for NEPC, with estimates up to 15% of men may develop this aggressive subtype of prostate cancer after hormonal treatment—a major problem because these men face very poor outcomes.
The team hopes that our study and lots of other research going on around the world will eventually lead to smarter, more targeted ways to treat NEPC or even prevent its emergence.
One author of the study is Associate Professor Luke Selth.
The study is published in Cell Reports.
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