PNAS: Important molecules promote invasive growth of human lung cancer

This important molecule is an enzyme called EphA2. The Salk team found that when EphA2 is mutated, the various systems in the cell lose control and rapidly develop into tumors. The work was published in the international academic journal PNAS, which showed that EphA2 could be further developed as a target for the treatment of a lung cancer subtype.

Professor Inder Verma said: "Sometimes there may be hundreds of genetic mutations in a patient's tumor cells, but you don't know which mutations are the driving factors of tumors and which are the by-products after tumors appear. We found one New ways to find cancer-suppressing genes can help us understand how to develop new targeted therapies based on these genes that express inhibitors."

The researchers first narrowed the study to thousands of genes that inhibit cell growth and proliferation, and then quickly and efficiently detected the role of these thousands of genes in tumor development through genetic screening. Through animal model studies, the researchers found that the synthesis of 16 genes can have a significant impact on KRAS and p53-associated tumors, and EphA2 is the most prominent one. Prior to the study, scientists have been unclear about the role of EphA2 in lung cancer, and the team found that EphA2 deficiency leads to more aggressive growth of KRAS-related tumors. In addition, the researchers also detected genetic alterations in EphA2 in patients with lung adenocarcinoma.

The researchers said that because EphA2 activation leads to inhibition of cell growth and proliferation signals, they believe that EphA2 may be a potential drug target for the treatment of KRAS-dependent lung adenocarcinoma. But they also pointed out that EphA2 does not always play a tumor suppressive role, its role may be dependent on the environment, so the design of targeted therapy according to EphA2 requires careful evaluation of the function of the molecule.