Secret Agent ML-7 Attacks Cancer Skeleton in Breast

Researchers are constantly looking for new ways to attack the cellular processes of cancer cells. Now researchers at the University of Illinois have focused on the cancer cell's skeletal structure, in an attempt to make cancer treatment safer and more successful.

A molecule that interferes with the internal scaffolding that shapes the cell may kill cancer cells, retard the growth of tumors and give a boost to a common chemotherapy drug, according to findings appearing in the May issue of the European Journal of Cancer.

Although tumor growth depends on the rapid cell division and mobility of cancer cells -- processes highly dependent on the cytoskeleton -- the cytoskeleton has not been a target in treating cancer, said Primal de Lanerolle, professor of physiology and biophysics at the University of Illinois at Chicago and principal author of the study.

The researchers found that ML-7, which inhibits an enzyme called myosin light chain kinase, which is important to the structure and dynamics of the cytoskeleton, induces cell suicide, or apoptosis, in cultured breast and prostate cancer cell lines. In addition, treatment with ML-7 in combination with etoposide, a chemotherapy drug used to treat solid tumors, enhanced the ability of etoposide to kill cancer cells.

In animal models, ML-7 retarded growth of breast cancer and prostate cancer tumors. The combination of ML-7 and etoposide reduced tumor growth by 88.5 percent for the breast cancer tumors and by 79.1 percent in the prostate cancer tumors compared to controls.
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In the fight against cancer it is important to focus specifically on tumour cells while sparing normal cells as much as possible. ML-7 appears safe, and may allow oncologists to use lower doses of toxic chemotherapy drugs, thus sparing body tissues that divide rapidly but are not cancerous, such as bone marrow cells and GI tract lining.