Scientists discover molecule that acts as natural cancer defense

Kathleen Blanchard's picture

Scientists from Canada have found a natural defense mechanism for cancer prevention. Cytokines have long been known to produce diseases that include cancer, diabetes, and chronic inflammation. The new study identifies a link between the SOCS1 molecule and the p53 gene that is found to be lost among a majority of cancer patients.

The new research surprisingly showed the link between SOCS1 molecule and cancer. According to a lead author and Université de Montréal student, Viviane Calabrese The research team didn't anticipate that SOCS1 would turn out to be linked to p53, the master regulator of natural anticancer defenses. We were surprised to realize that SOCS1 was directly linked to p53."

The p53 gene is a natural tumor suppressor and is also linked to cancer causing cytokines. The new research shows that loss of the SOCS1 molecule also disables the P53 gene, thus disabling the body's natural defenses against cancer.


When the researchers reintroduced the SOCS1 molecule into cancer cells, the tumors became dormant. The SOCS1 molecule prevented cancer cells from multiplying, producing a state known as cell senescence.

Dr. Gerardo Ferbeyre, senior author and a Université de Montréal biochemistry professor explains, "Discovery of these mechanisms will enable scientists to design a cancer-prevention strategy for people with chronic inflammatory diseases and lead to better understanding of the human body's natural defenses against cancer."

The SOCS1 molecule is now found to be an important natural defense against cancer, and directly linked to the p53 gene that is lacking in patients who develop cancer. By reintroducing the SOCS1 molecule into tumor cells, the researchers found they could prevent cancer cells from multiplying, placing cancer cell in a dormant state.

Activating natural cancer defenses by targeting the SOCS1 molecule for individuals with chronic inflammatory diseases could lead to new strategies for cancer prevention.

Cell Metabolism