Prostate cancers often can be treated by hormone therapy: lowering the amounts of dihydro-testosterone can effectively reverse prostate cancer, if administered early enough in the progression of the cancer.  However, if the cancer is not detected until a later stage, the cells can become “castration-resistant” (CRPC); meaning the cells can survive and continue to proliferate without dh-testosterone.  This stage is highly problematic and necessitates a new target for therapy.

During EMT (epithelial-to-mesenchymal transition), the cancer cells acquire attributes allowing them to migrate and establish at new sites (or metastasize, the most dangerous progression of cancer).  This study examined the EMT process by looking at a likely suspect: Hsp27.  High-levels of Hsp27 are known to be associated with advanced stages of several cancers.  Specifically, these researchers collected evidence that expression of Hsp27 increased cell migration and matrix metalloproteinase (MMP), which promote tumour migration and metastasis.  Further, they conducted experiments whereby Hsp27 was silenced using shRNA  (sh-Hsp27).  The results from this silencing of Hsp27 showed cells that did not exhibit the changes associated with EMT; there was less cell invasion, MMP activity and migration.

These researchers postulate that Hsp27 is a key regulator of this critical EMT phase, and is therefore a new possible target for treatment.

The original research paper was published in: Cancer Research, (online March 14, 2013).

Hsp27 Regulates Epithelial Mesenchymal Transition, Metastasis and Circulating Tumour Cells in Prostate Cancer.