Researchers Discover New Functions of PARP-1 Inhibitor in Treating Advanced Prostate Cancer

October 10, 2012 by  
Filed under Prostate Cancer News

PARP-1 is known to help in repairing damage to DNA. Now, scientists have discovered another vital important function of Inhibitor.

This function is the regulation of Androgen Receptors (AR) to control advanced prostate cancer growth.

Researchers from the Thomas Jefferson University discovered this new function and the findings of their study have been published in the Cancer Discovery.

Details of the preclinical study and the basis of the dual functions of the PARP-1 inhibitors are detailed in the extract below:

A newly discovered function of PARP-1 could be the key to more effective therapeutics to treat advanced prostate cancer patients, a recent preclinical study published in Cancer Discovery by Jefferson’s Kimmel Cancer Center researchers suggests.

The team, led by Karen E. Knudsen, Ph.D., Professor in the Departments of Cancer Biology, Urology, & Radiation Oncology at Thomas Jefferson University, found that functions of PARP-1 not only include DNA damage repair but also androgen receptor (AR) regulation in advanced prostate cancer growth and progression. PARP inhibition in various models was found to suppress AR activity, which fuels prostate growth. Researchers believe that the dual functions of PARP-1—as both a regulator of AR as well as critical for DNA damage repair—could be leveraged for therapeutic benefit. PARP inhibitors could slow down advanced-stage prostate cancer and shrink tumors, the team surmises.

“We hope to capitalize on this previously unknown function in PARP-1 in prostate cancer,” said Dr. Knudsen. “Our data show that PARP-1 plays a major role in controlling AR function and that, when suppressed with inhibitors, enhanced anti-tumor effects of castration and delayed onset to castration resistance. ” “This is the basis to support a clinical trial investigating PARP-1 inhibitors in patients with advanced disease,” she added.

Today, PARP-1 is seen as a valuable target because of its involvement in DNA damage repair for cancer cells. The therapy has been successful when combined with DNA-damaging drugs because it heightens the apoptotic activity of these drugs. In other words, it helps halt tumor growth by stopping DNA repair in various cancers. Prostate cancer is dependent on AR activity for growth and survival, and is largely resistant to standard chemotherapy. AR-directed therapies are the first-line intervention for patients with advanced disease; however, recurrent tumors arise when AR is reactivated, a common occurrence in the castrate-resistant stage of the disease.

Therefore, there is a dire need to develop means to suppress the AR function in these patients. With this new role defined, PARP inhibitors targeting both functions could sensitize prostate cancer cells to DNA damage, and potentially improve the efficacy of AR-directed therapies in these patients, the researchers suggest in the paper. Almost 40 percent of men with prostate cancer progress into an advanced stage, termed castrate-resistant prostate cancer, where chemotherapy and other therapies have little to no effect.

Using various in vitro and in vivo model systems, the researchers found that PARP-1 activity is required for AR function and is increased in castrate-resistant prostate cancer. Additionally, inhibiting PARP-1 suppressed proliferation of cultured, primary human tumor specimens in a state-of-the-art system. “These findings introduce a paradigm shift with regard to PARP-1 in prostate cancer,” said Dr. Knudsen, “and provide the basis for new therapies that could help a whole population of cancer patients who have little options.” Click here to read the concluding details.

This new study is a step forward in prostate cancer research. It indeed represents a new paradigm shift with the function of the PARP-1.

The dual functions will readily help to treat advanced level prostate cancer with ease. At least, this can lead to better therapeutic treatments to curtail the growth and progressions cancer originating from the prostate gland, which is becoming aggressive.

Hopefully, new therapies would be developed fast towards that area based on the discovery of the new function of the PARP inhibitors.

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