Jan. 13 (UPI) -- Researchers may have found how some skin cancer cells become resistant to currently available chemotherapy.
In a study published Monday in the journal Cancer Cell, researchers from Queen Mary University of London describe how melanoma cells fight anti-cancer drugs by changing their internal skeleton, or cytoskeleton.
The discovery could open up new treatment options to combat skin and other cancers that develop resistance to treatment, they say.
"In a nutshell if you are a cancer cell, what does not kill you makes you stronger," lead author Victoria Sanz-Moreno, professor of cancer cell biology at Queen Mary, said in a statement.
According to the Melanoma Research Alliance, melanoma is the most diagnosed cancer among 25- to 29-year-olds in the United States. An estimated 6,850 people in the U.S. are expected to die of melanoma in 2020 -- about 4,610 men and 2,240 women.
Essentially, Sanz-Moreno and her team found in tests with mice that melanoma cells stop responding to both immuno-therapies and drugs targeted at the tumor's faulty genes -- typically B-RAF or N-Ras mutations in the MAPK pathway -- by increasing the activity of two cytoskeletal proteins -- ROCK and Myosin II. These proteins effectively enable cancer cells to develop new "skins" that protect them against anti-cancer drugs.
ROCK and Myosin II have both been previously linked with the metastatic spread of melanoma. According to the authors of the current study, this suggests there is a strong connection between metastasis and therapy resistance -- confirming that the cytoskeleton is important for determining how aggressive a cancer is.
The team also discovered that blocking the development of ROCK-Myosin II not only reduces cancer cell growth, but attacks faulty immune cells that are failing to kill the tumor. This action boosts anti-tumor immunity.
They also noted that resistant human melanomas had increased levels of Myosin II activity, which suggests the protein could be a potential biomarker for treatment failure. Resistant melanomas also had increased numbers of faulty immune cells, which may contribute to the lack of response, they added.
"We were very surprised to find that the cancerous cells used the same mechanism, changing their cyto-skeleton, to escape two very different types of drugs," Sanz-Moreno said. "However, their dependence on ROCK-Myosin II is a vulnerability that combination drug therapy tests on mice suggest we can exploit in the clinic by combining existing anti-melanoma therapies with ROCK-Myosin II inhibitors."