If prostate cancer does not give up, it is destroyed by blocking the Stat5 gene

Usually, primary prostate tumors are surgically removed or treated with radiotherapy, and secondary tumors are treated with hormonal drugs. However, in cases where the tumor occurs again, after a few years, it can be much more aggressive and does not respond to hormone therapy, often leaving no chance of a cure.

Jefferson's Kimmel Cancer Center (Philadelphia) scientists, working under the guidance of Dr. Marja Nevalainen, demonstrated on cell culture and on an experimental animal model that blocking the Stat5 signaling protein, which plays a key role in the process of tumor growth, destroys hormone-resistant prostate cancer cells.

Starting the work, the authors aimed to prove the key role of the Stat5 gene in the viability of prostate cancer cells. They blocked the expression and functions of this protein by several methods, including inhibition using small interfering RNA (miRNA), antisense inhibition, and delivery of the inhibitory form of the Stat5 gene into cells using adenovirus. All methods resulted in the death of tumor cells in culture. In addition, blocking the expression of the Stat5 gene prevented the formation of tumors in mice that had previously been implanted with prostate cancer cells.

This proves the value of the Stat5 gene as a therapeutic target for the fight against prostate cancer, especially with difficult-to-treat forms of the disease.

The authors demonstrated that the Stat5 gene is active in almost all recurrent prostate tumors resistant to hormone therapy. In addition, they found that the cause of the aggressiveness of such tumors is the fusion of Stat5 and androgen receptor.

Currently, scientists are looking for ways to use Stat5 as a therapeutic target for the treatment of hormone-resistant prostate cancer and at the same time are testing the hypothesis that blocking this gene can increase the sensitivity of tumors to traditional treatments such as chemo and radiotherapy.

Portal "Eternal youth" www.vechnayamolodost.ru based on the materials of ScienceDaily

04.03.2008