Diabetes drug may activate molecule that triggers cancer growth

Scientists studying the effects of the diabetes drug metformin on treating a variety of cancers in various clinical trials previously have cited the activation of a molecular regulator of cell metabolism—AMPactivated protein kinase (Ampk)—as suppressing tumor growth. However, a new study suggests that the activation of AMPK may actually fuel cancer growth.

The study's leaders, from Cincinnati Children's Hospital in Ohio, also suggest that researchers working on clinical trials of metformin and cancer carefully evaluate their clinical data. They are not saying that these trials should be stopped, but rather, that the drug's mechanism of cancer suppression is unclear.

The Cincinnati researchers reported on extensive laboratory tests indicating that metformin does stop cancer, but not by activating AMPK. The tests, on glioblastoma cells, found that the drug inhibits a molecule called mammalian target of rapamycin (mTOR), which has been linked to many cancers. Metformin also suppresses the action of insulin and insulinlike growth factors, which support cancer growth. Their studies also found that AMPK potentially works as a tumor growth supporter and that researchers studying metformin in cancer clinical trials should be cautious in interpreting their data.

The researchers conducted experiments involving laboratory cell cultures of human glioblastoma cells and glioblastoma tumors transplanted in mice. Compared with normal human and mouse tissue, the researchers found that AMPK was highly active in human and mouse glioblastoma cells. They then treated the cancer cells with metformin and conducted a series of genetic tests to determine the molecular pathways it uses to stop the cancer growth. Those tests showed clearly that metformin directly inhibited the mTOR pathway and the cancer by promoting the interaction of 2 upstream molecules that stop the pathway's function.

Malignant melanomas that arise from the iris, ciliary body, and choroid layers of the eye-collectively referred to as uveal melanomas—represent the most common primary cancer of the eye and the second most common form of melanoma. Until recently, the identification of effective therapies for metastatic uveal melanoma has been hampered by a lack of known driver mutations. This situation has changed in recent years with the discovery of several common driver mutations, which has opened the door to rational targeted therapies.

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