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Von Hippel-Lindau protein suppressed androgen receptor activity
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A function of the von Hippel-Lindau protein within the androgen receptor may play a critical role in the development of prostate cancer. This novel finding could help researchers develop an understanding of the underlying mechanism for prostate cancer, according to data published in Molecular Endocrinology.
The von Hippel-Lindau gene (pVHL) is known as a classic tumor suppressor that, when activated, could suppress androgen-induced cell proliferation, according to researchers of The Key Laboratory of Aquatic Biodiversity and Conservation at the Institute of Hydrobiology and Chinese Academy of Sciences in Wuhan, China.
They performed luciferase reporter assay, semiquantitative real-time polymerase chain reaction, Western blot and immunoprecipitation assay, glutathione S-transferase pull-down assay, and cell growth assay; and found that pVHL interacts with androgen receptors in vitro and in vivo.
In addition, pVHL inhibited androgen receptor transactivity, induced deubiquitination of androgen receptors, and inhibited androgen-induced cell proliferation.
“As a classic tumor suppressor, multiple lines of evidence show that dysfunction of pVHL is crucial for development of clear cell renal cell carcinomas, hemangioblastomas and pheochromocytomas,” researchers wrote.
These data indicate that pVHL interacts with androgen receptors by suppressing the transactivity of androgen receptors; and inhibits cell proliferation by inducing deubiquitination of the receptors.
Further studies are warranted to explore the deregulation of pVHL and its role in the development of prostate cancer, researchers wrote.
Disclosure: The researchers report no relevant financial disclosures.
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