Protein imbalance leads to cancer, and gene mutation theory is subverted again!

Genetic abnormalities have long been thought to be the main cause of cancer, but a new study has found that protein imbalance in cells can lead to cancer Scientists say this is a major breakthrough, revealing the non genetic mechanism of cancer The results, published in oncogene, show that protein imbalance is a powerful cancer prediction tool, which can determine whether patients respond to chemotherapy or whether the tumor spreads to other parts The results open the door to new cancer therapies that target measurement and prevent cell imbalance Cancer caused by imbalance of two proteins Under normal conditions, cells receive external signals through cell wall binding receptor (FGFR2) After being stimulated, the receptor is opened in the cell, so as to start the signal protein and protein kinase pathway and realize cell proliferation In some cancer cells, this pathway is permanently open The traditional way of cancer diagnosis is to find a genetically modified receptor, which is responsible for keeping the cellular protein pathway open Led by the University of Leeds and MD Anderson Cancer Center at the University of Texas, the team focused on the research of "Akt signaling pathway" - protein kinase pathway, an intracellular signaling pathway that drives cancer formation and tumor transmission in vivo The researchers observed the changes of cancer cells without external stimulation, and found that "Akt signaling pathway" can also be activated without genetic modification Plcy1 and Grb2 compete for binding to FGFR2 receptor The relative concentration of protein determines which protein wins the competition It is found that when the content of plcy1 is high, Akt signal pathway will be triggered In this way, the imbalance of the two proteins can lead to cancer cell proliferation and tumor formation Dr Zahra timsah, the lead researcher of this study, said that the competition between different proteins and receptors could cause cancer was unexpected The study also found that FGFR2 receptors are more likely to bind to plcy1 when the Grb2 protein in cells is depleted, which can lead to uncontrolled spread of cancer But when the content of Grb2 was increased, the uncontrolled situation was reversed and the normal activity of FGFR2 was restored The researchers believe that under normal circumstances, the fair competition between the two proteins and the normal binding of plcy1 receptor are the useful stewards of cells, but when the protein imbalance will lead to the loss of control of plcy1, further leading to the formation of tumors The researchers also found that the loss of Grb2 led to the development of multiple tumors near the main tumor, which indicated that the protein imbalance played a role in the tumor diffusion process This makes sense, because plcy1 plays a role in cell movement The researchers used the imbalance of Grb2 and plcy1 to predict breast cancer, and found that higher Grb2 level means better prognosis and longer survival time of breast cancer Single gene screening is not enough -- non genetic factors or the key to understanding cancer Professor John ladbury, the first author of this paper and Dean of the school of Biological Sciences at the University of Leeds, said that human genome sequencing has become a huge investment, and people have always had the idea that if we know all the genetic information, we can predict the risk of cancer, and finally use the treatment based on the development of precision medicine But our research shows that single gene screening is not enough Previous studies have emphasized that the root cause of cancer is gene mutation Some studies have shown that cancer is not affected by genetic factors, such as epigenetic modification of proteins But the study showed that receptors can also transmit signals when they are not activated, so non genetic factors may be the key to understanding cancer The team is currently working with clinicians at the University of Leeds on non genetic mechanisms for other cancers They are exploring whether other cell receptors, like FGFR2, can produce tumor signals when they are not activated.