Researchers at Columbia University Medical Center (CUMC) have found that fusion of two adjacent genes, FGFR3 and TACC3, causes excessive mitochondrial movement, which provides energy for rapid cell growth and is carcinogenic. They published a paper in the online edition of Nature recently, which showed that targeted drugs targeting this consistent cancer factor can prevent tumor growth. The study provides new ideas for the treatment of cancer caused by genetic fusion.
As early as 2012, CUMC researchers found that some glioblastomas are caused by the fusion of FGFR3 and TACC3 genes. Since then, many scientists have found the same genetic fusion in some cancer cases such as lung cancer, esophageal cancer, breast cancer, cervical cancer, and bladder cancer, but the mechanism by which this fusion promotes tumor growth has not been clarified.
This time, CUMC researchers found that the fusion of these two genes activates a protein called PIN4. Once activated, this protein causes a multiplication of peroxisomes and releases a large amount of oxidant. These oxidants induce a key regulator of mitochondrial metabolism, PGC1alpha, which causes excessive movement of mitochondria, which produces the large amount of energy required for rapid cell division and growth.
The researchers found that treatment of human brain cancer cells containing FGFR3 and TACC3 genes by mitochondrial inhibitors blocked energy production in cancer cells and significantly slowed tumor growth. Experiments against a mouse model of human brain cancer containing this gene fusion also showed the same results.
New research shows that drugs that directly target mitochondrial metabolism and FGFR3 and TACC3 genes may avoid tumor recurrence caused by drug resistance. For the treatment of cancer caused by gene fusion, dual treatment with mitochondrial inhibitors and kinase inhibitors may Will be effective. (Technology Daily)
Rechargeable Solar Camera,Night Vision Monitor,Solar Cctv Camera,Wireless Security Camera
Shenzhen Zuomi Technology Co., Ltd. , https://www.bkvis.com