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Novel Molecule That Induces Cancer-Killing Protein Identified By New Study

Novel Molecule

Even after several years of research that has gone into finding a permanent cure to cancer, a final solution to the problem is yet to be seen. Cancer has baffled researchers for long and continues to do so even do. Even though our fight against cancer has gone from strength to strength, there is a lot about it that remains a mystery.

 

In a recent study that was conducted in the University of Kentucky, researchers have got some breakthrough that could help in finding a treatment to cancer. They have identified a novel molecule which has been named Arylquin 1 as a potent inducer of Par-4 secretion from normal cells. Actually, Par-4 is a protein that acts as a tumor suppressor and is known to have the power to kill cancer cells without harming any normal cells in the body. The normal cells in the human body do secrete a small amount of Par-4 on their own, but that amount is quite tiny and is not enough to kill cancer cells. It is noted that if the secretion of Par-4 is suppressed, the tumor growth is enhanced.

 

For this study that was published in The Nature Chemical Biology experiments were carried out in lab cultures and animal models. It revealed that low levels of Arylquin 1 induced Par-4 secretion without causing harm to the producer cells. The researchers also found that Par 4 is bound to a protein called vimentin which has a role to play in tumor metastasis. Arylquin 1 works by binding to vimentin; it displaces the Par-4 for secretion “ so, it is likely that it can also be useful for inhibiting the spread of cancer.

 

Researchers believe that these finding can have a very strong implication for the development of future cancer treatment. Focus is now on the development of Arylquin 1 in the form of a drug that could inhibit both primary and metastatic tumors.

 

Finding a cure for cancer has been difficult because there is no scan or test that can effectively detect a cancer cell. In fact, a group of cancerous cells can remain dormant for years and can easily go undetected. These undetected cells have the chance to form tumors. When these tumors and cells spread in the body, the cancer is said to have metastasized. The irony is cancer is mostly detected after it has spread in the body which makes it even difficult to treat it.

 

Since, there has not been any breakthrough in finding a way to detect cancer cells early; stress is being given to finding a way to treat the cancer cells. Cancer therapies such as radiation and chemotherapy primarily target and kill cancerous cells in the midst of division. But, the problem often remains as some cancerous cells lie dormant for long periods of time and survive several rounds of treatment. That’s why we often hear that cancer can come back years after the treatment.

 

Vivek Rangnekar, UK professor and Alfred Cohen Chair in Oncology Research in the Department of Radiation Medicine, says that – “We found that Par-4 is inactivated by pro-metastasis proteins such as vimentin, which implies that by using small molecule drugs that target metastasis proteins, we may be able to both inhibit the spread of cancer while also releasing the tumor suppressor – Par-4 – to then induce the death of the cancerous cells.”

 

Rangnekar also serves as the Associate Director for the UK Markey Cancer Center. He had initially discovered the Par-4 gene in 1994. Today, he is working closely with UK medicinal chemist David Watt and a multidisciplinary team across the UK campus and is working on developing secretagogues that can cause elevated secretion of Par-4 for the inhibition of primary and metastatic tumors.


This study was funded by grants from the National Cancer Institute, the National Center for Research Resources and the UK Center for Clinical and Translational Science.

 

 

References

 

http://uknow.uky.edu/content/uk-study-identifies-molecule-induces-cancer-killing-protein

http://www.counselheal.com/articles/11226/20140908/researcher-identify-molecule-induces-cancer-killing-protein.htm