The nucleolar protein NIFK promotes cancer progression via CK1α/β-catenin in metastasis and Ki-67-dependent cell proliferation

Cancer cells can rapidly divide to form a tumor. Small groups of cells can leave the tumor to migrate to other sites in the body, and it is these “secondary” tumors that are often responsible for the death of cancer patients. Many proteins influence how and when cells divide and migrate. One such protein called Ki67 is only produced when cells are dividing and it is often used in the clinic as a marker to indicate whether cells have become cancerous. However, it is not clear how Ki67 regulates the progression of cancer. Ki67 interacts with another protein called NIFK, and Lin, Su et al. have now investigated the role of NIFK in cancer. First, publicly available data on the levels of proteins in tumor samples from cancer patients were analyzed. This revealed that, in several different types of cancer, tumors that produced more NIFK were more likely to spread to other parts of the body than tumors that produced smaller amounts of NIFK. Next, Lin, Su et al carried out experiments using human lung cancer cells. This revealed that cells that produced larger amounts of NIFK were more likely to migrate, while cells with lower levels of NIFK divided and migrated less often. Further experiments showed that NIFK increases the activity of genes that are involved in cell migration. NIFK achieves this by reducing the production of a protein that inhibits the activity of another protein called β-catenin. Lin, Su et al.’s findings reveal a new role for NIFK in promoting the development of cancer. A future challenge is to find out whether chemicals that inhibit NIFK could be used in the treatment of lung cancer.