Scientists Target Protein to Lower the Risk of Prostate Cancer Proliferation
Proteins and prostate cancer
According to a study led by Cedars-Sinai Cancer investigators, targeting a particular protein that is often overexpressed in prostate cancer can help avoid or postpone the disease from infecting other parts of the body.
The research study, released in the peer-reviewed journal Nature Communications, opens up the prospect of using available commercial drugs. This includes one accepted by the Food and Drug Administration for leukemia, to shut down a protein called receptor-interacting protein kinase 2– or RIPK2. If confirmed in human clinical trials, the finding might have a major influence on the treatment of males with advanced prostate cancer.
” About 90% of cancer fatalities are brought on by the reoccurrence of metastatic cancer, which occurs when cancer infects other organs,” stated Wei Yang, Ph.D., associate professor of Surgery and Biomedical Sciences. “So, if we can stop the occurrence of metastatic cancer, we can substantially prolong the lives and enhance the quality of life for males with this disease.”
To much better comprehend the genetic drivers of disease development and potential treatment targets, the Cedars-Sinai team examined the molecular profiles of cancer tissue in males with advanced prostate cancer. The investigators discovered that RIPK2 was increased in about 65% of lethal prostate cancers, which kill roughly 34,000 U.S. males yearly.
” We discovered the amplification of the protein RIPK2 boosted together with cancer progression, which showed us that this protein might have a crucial role in cancer progression,” stated Yiwu Yan, Ph.D., a project researcher in the Yang Laboratory and first author of the study.
This protein has been studied in inflammatory disorders. However, little is known about its molecular functions in the context of cancer progression and metastasis, Yang said.
Prospective solutions
Once the protein was identified, the group performed a large-scale analysis to aid decode just how RIPK2 could modify the activity of other functions in the cell. Investigators discovered that RIPK2 activates another protein, which consequently causes a vital driver named c-Myc that fuels the progression and metastasis of numerous cancer types, including prostate cancer.
In a string of experiments in mice, investigators found that inhibiting the RIPK2 function with both small molecular inhibitors (drugs) and a gene-editing system– referred to as CRISPR/Cas9– substantially reduced the spread of prostate cancer.
They discovered that targeting RIPK2 with ponatinib, an existing FDA-approved protein inhibitor, lowered prostate cancer metastasis by 92% in mice.
” Administrating RIPK2 small molecular inhibitors is a high-value approach that decreased the metastasis in mice by over tenfold,” Yang stated. “If we can apply this to human patients, we may extend patients’ lives by multiple years, instead of just many months.”
The following step is to identify biomarkers that can aid guide investigators and clinicians to choose the team of patients that would benefit most from this therapy. Additionally, investigators will undoubtedly evaluate the results of RIPK2 inhibition on immune cells to see if the protein can potentially boost immune cells’ capability to attack tumors.
“Targeting RIPK2 in preselected patients, either alone or combined with conventional or emerging treatments, could hold the capacity for boosting the survival time and quality of life of cancer patients,” Yang claimed.
Read the original article on Medical Xpress.
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