A research from Baylor College of Medicine claims that a novel technique of obstructing the origins of blood vessels that nourish tumors may begin with the nuclear receptor COUP-TFII i.e. chicken ovalbumin upstream promoter-transcription factor II. A set of researchers headed by Dr. Ming-Jer Tsai and Dr. Sophia Y. Tsai, both professors of molecular and cellular biology at BCM, supposedly defined the experiments in which the development of new blood vessels and tumors themselves were said to be repressed when COUP-TFII was not there.
The research illustrates that the receptor seems to control an angiogenic factor known as Angiopoietin-1, which appears to improve the growth of new blood vessels. Devoid of COUP-TFII, Angiopoietin-1 apparently does not perform its work capably, which means that neither the blood vessels nor the tumors develop, perhaps since there is inadequate vasculature to offer nourishment.
Dr. Ming-Jer Tsai, commented, “This is important because it means we may be able to find an antagonist that can intervene to halt tumor growth and metastasis. Metastasis is the reason most cancer patients die.”
Currently, various researches of vascular endothelial growth factor (VEGF) inhibitors are ongoing. This factor could also play a significant function in the development of new blood vessels. Also the drugs seemed to function against the tumors only for sometime.
He mentioned, “They only work on one pathway of angiogenesis.”
This outcome appears to recognize a new vital pathway and a different method to combat the tumors.
One more advantage of knocking out COUP-TFII is that apparently it is not required in adult animals. COUP-TFII is claimed to be the most imperative in blood vessel development in the growing fetus. But it supposedly plays no vital position in preserving the vasculature later, apart from in conditions like pregnancy or wound healing. The blood vessels of adult animals that are said to not have the factor supposedly stayed normal.
The findings were published in the Proceedings of the National Academy of Sciences.