Ponatinib an FDA-Approved Drug  Inhibits RIPK2 a Protein Involved in Prostate Cancer Metastasis

Prostate cancer is the most common cancer that threatens the lives of many men across the globe today. Occurring in over 34,000 men in the U.S alone, doctors are finding it quite difficult to manage, as its metastatic character (a character that is peculiar to every cancerous cell), makes it incompletely removed from the body from the patient, even when they resort to surgery involving the removal of these cancerous outgrowths. Sometimes, by the time the cancer is discovered, it has already spread to other organs, and by the time it is been removed, there is still a chance for cancer recurrence in the patient due to the initial spread of cancer to other organs. This has been the common issue with people suffering from this condition and is the reason for the death of so many. Perhaps, if cancer did not spread, there may be a higher chance of survival after the infected cells have been gotten rid of.

Prostate Cancer

Histological Slide Showing Prostate Cancer

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Scientists have been making research to see if this is possible; they have been working to find a way to make cancer cells remain restricted to only the initial area where they began; to prevent their spread. And according to recent findings of the research led by Cedars-Sinai Cancer Investigators, yes, it is possible.

The Study

The research team examined the cancer tissues in several men with advanced prostate cancer, and they discovered that a protein was always present in all cases and that the amount of the protein was even higher in about 65% of the prostate cancer cases that led to death. In previous research, this protein, known as receptor-interacting protein kinases 2, RIPK2, was found to be linked to inflammatory disorders, however, not much is known about its molecular structure and function.

Therefore, this discovery made scientists dig deep into the molecular composition of this protein. They observed that this protein was linked to stimulating the development of diseased cells, genetically, within the tissues of the examined cases. This implied that RIPK2 is the major contributor to the spread and progress of the cancer cells within the body’s organs. As they studied the protein further, they were able to understand the working mechanism of this protein: RIPK2 causes another protein to be active, thus, initiating another key driver known as c-Myc, that facilitates the spread of not only prostate cancer cells, but also, those of many cancer types.

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To determine ways to halt the action of this protein, they carried out another experiment to test the effect of some drugs known to be protein inhibitors, on mice. They also tried the gene-editing system (CRISPR/Cas9) on these animals, in an attempt to determine how the spread can be inhibited. In both cases, the results were positive – it was possible to halt the action of RIPK2 using both techniques. Another trial included the use of the existing FDA-approved protein inhibitor – ponatinib – and this also proved effective. Thus, scientists are now working to replicate the same in humans in a way that would be safer, producing little or no side effects.

Clinical significance

Cancer is one of the most life-threatening disease conditions to humanity today, and this study has opened a new page that contains vital information on how to effectively treat, and maybe cure it too.

When these scientists eventually manufacture those protein-inhibiting drugs, it may mark the beginning of the end of the war with not just prostate cancer, but many cancer types too since the cancer cells have a peculiar character.

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The discovery in this study is a hope to the world of medicine, as no cure has yet been discovered for this life-threatening condition. Perhaps, this is the limelight that will eventually push cancer off the stage.


Receptor-interacting protein kinase 2 (RIPK2) stabilizes c-Myc and is a therapeutic target in prostate cancer metastasis



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