ANRIL has been found to be dysregulated in a variety of cancers such as breast cancer, prostate cancer, and gastric cancer. Its overexpression or aberrant functioning can lead to the silencing of tumor suppressor genes, thereby promoting cancer cell survival and proliferation. For instance, ANRIL can recruit Polycomb Repressive Complex 2 (PRC2) to the INK4 locus, leading to the epigenetic silencing of p15INK4b and p16INK4a, which are essential for cell cycle regulation.
