According to a study published today in Nature Communications, PTEN, a tumor suppressor gene mutated in many prostate cancers, relies on another gene to function. This new discovery provides a potential therapeutic target for prostate cancers carrying the common PTEN mutation.

“Loss of the tumor suppressor PTEN due to mutation or deletion not only is frequent in human prostate cancer, but also plays a large role in other cancers. We wanted to find out more about PTEN, and other genes it might rely on, to offer new treatment options for those with the PTEN mutation,” says first author Ray-Chang Wu of George Washington University. “We discovered that PTEN has an important connection to the gene ARID4B, which offers a new therapeutic target for treatment.”

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The team examined data from several prostate cancer cohorts and made an interesting observation: Cancers that contain PTEN mutations almost always retain ARID4B. One function of the gene ARID4B includes remodeling the chromatin that makes up the chromosome. This “mutually exclusive” pattern between PTEN and ARID4B offers the first clue as to its potential importance in prostate cancer.

The researchers also found that suppression of ARID4B expression in cancer cells with the PTEN mutation significantly inhibits cancer cell growth and increases cell death. In comparison, less pronounced effects were observed when cancer cells that contain functional PTEN were used, suggesting a dependence on ARID4B by PTEN-deficient prostate cancer.

Importantly, the team was able to recapitulate these findings using the PTEN-deleted prostate cancer mouse models. As expected, deletion of PTEN alone in mice leads to the development of prostate cancer. In stark contrast, mice with deletion of both PTEN and ARID4B do not develop tumors. Collectively, these results led the team to conclude that PTEN function depends on the presence of ARID4B, meaning that ARID4B could potentially be used as a potential therapeutic target for certain types of prostate cancer in the future.