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A new mechanism of prostate cancer growth was discovered

 
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Last reviewed: 23.04.2024
 
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16 August 2012, 09:26

Specialists of the Cancer Center of the United Kingdom have opened a new path through which male androgen hormones stimulate the growth of the tumor of the prostate gland.

The results of the study, published in the journal Molecular Endocrinology, suggest that some of the existing drugs can be used to effectively treat this disease.

Prostate cancer is most often treated with hormone therapy, which targets the androgen receptor (AR), a large protein that includes a signal path that causes the cell to divide. As you might expect, it is this protein that exhibits irreducible activity in the tumor cells. However, the AR receptor does not act in a vacuum, but in a particular ecosystem, in contact with proteins such as HSP90 and p23 that help it to fold into an activated form.

Previously it was thought that p23 and HSP90 should work in pairs in order to run AR, but the current study claims that p23 lives and creates by itself, regardless of possible partners in the shop increasing AR activity.

From this seemingly unpredictable discovery, a simple but very important consequence follows: a drug that blocks p23 activity can be an effective treatment for prostate cancer that is immune to HSP90 blockers. Moreover, such therapy can be much more effective.

Fortunately, drugs that can stop p23, there - for example Celastrol, a drug of natural origin (come to us from traditional Chinese medicine). Celastrol has already shown its usefulness in the treatment of arthritis and asthma - which means that even today it can be launched into a series of clinical trials on cancer patients.

To establish the independent role of p23 in AR receptor activation, scientists used a modified version of the latter, unable to bind to HSP90, and (as a reference for comparison) a modified p23 that can not bind to AR. The result of such combinations here is the conclusion that intermediaries are not needed to run the AR of the p23 protein.

trusted-source[1], [2], [3], [4], [5]

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