How a Silent Gene Switch Can Boost Cancer Growth

The RINES gene, normally hidden in a DNA region rich in CG pairs, can be turned off by adding methyl groups. When this happens across many cancers—esophagus, nose‑area, colon, breast, lung, kidney, cervix and liver—the result is a sharp drop in RINES protein. Patients whose tumors show this switch tend to do worse, suggesting the gene normally fights cancer. RINES belongs to a family of proteins that attach small tags called ubiquitin onto other proteins, marking them for destruction. In laboratory experiments, cells that keep RINES active grow more slowly and show fewer traits of “cancer stemness, ” the ability to keep multiplying and resist drugs. The opposite is true when RINES is missing or silenced.

The protein works by grabbing two key players in cancer—STAT3 and MYC—and tagging them for breakdown. Without RINES, STAT3 and MYC become more stable, piling up in the cell and driving it toward a stem‑like, aggressive state. Scientists proved this by cutting RINES out of cells: the tags on STAT3 and MYC disappeared, their levels rose, and cancer‑stem cell markers increased. Because RINES is so crucial for keeping STAT3 and MYC in check, it acts as a true tumor suppressor. Its loss removes an important brake on cancer growth and stemness, allowing tumors to spread more easily. Researchers are now looking at RINES methylation as a possible blood or tissue test. If a patient’s tumor shows the gene turned off, doctors might predict a higher risk of aggressive disease and consider more intensive treatment.

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