Many cancer patients develop new tumors that regenerate in the same area or metastasis (spread) to other body parts. It may occur in some years or decades after their initial therapy. Individual tumor cells that have been latent for lengthy periods before start growing again after being reactivated. They generate these secondary tumors, which are generally resistant to treatment. Relapse in patients may thus be avoided if researchers could develop a mechanism to retain cancer cells in a dormant state.
A new therapeutic strategy could accomplish this idea. It has the ability to stop the spread of metastatic tumors by putting cancer cells into a dormant condition where they can't replicate. The research is a breakthrough for the Circulating Tumor Cells Market as it could lead to novel treatments to prevent the recurrence or spread of cancers such as breast cancer and Head and Neck Squamous Cell Carcinoma.
The present study identifies a protein called NR2F1. It is responsible for regulating cancer cells' ability to remain dormant. This receptor protein can reach the nucleus of a cell and trigger a mechanism that prevents cancer cells from multiplying by turning many genes on or off. In original tumors, NR2F1 levels are generally modest. However, they are high in latent dispersed cancer cells. When cancer is present, levels of the NR2F1 protein drop again.
Teams used a computer-assisted screening method to find C26, a medication that activates NR2F1. C26 treatment of patient-derived HNSCC cells increased NR2F1 levels and slowed cell proliferation, according to the researchers.
As per the study, C26 activates NR2F1 and causes cancer cells to enter a long-lasting dormancy characterized by a distinct pattern of gene activity. Patients with tumors that have a similar pattern of gene activity had fewer relapses, implying that activating this dormancy program with C26-type medicines could be useful in humans.
Drugs that activate NR2F1 could be very beneficial in breast cancer. Activating NR2F1 may be able to prevent the reawakening of dormant cancer cells kept in that state by anti-estrogen therapy. This is because it is considered abundant in ER-positive tumors when compared to ER-negative tumors. Since C26 treatment raises -NR2F1 levels, it could be effective for other tumors with low levels of the receptor protein.
Overall, the research offers a mechanism-based and rationally conceived method for using NR2F1-activated dormancy as a treatment option to avoid metastatic relapse.