New York: A compound initially developed to reduce cholesterol molecule levels can not only halt the progression of prostate cancer but can also kill the deadly cancerous cells in the human body, a new study shows.
The findings suggest that the potential cholesterol drug, when used in combination with commonly used chemotherapeutic drugs, could represent a new therapeutic approach in the fight against prostate cancer, the researchers said.
The compound was found to be effective in reducing human prostate cancer cell growth.
Also, subsequent studies revealed that it caused cancer cell death.
“Often, cancer patients are treated with toxic chemotherapies; however, in our study, we focused on reducing the production of cholesterol in cancer cells, which could kill cancer cells and reduce the need for toxic chemotherapy,” said Salman Hyder, professor at University of Missouri in US.
Currently, treatment for primary prostate cancer includes systemic exposure to chemotherapeutic drugs that target androgen receptors located in the cancer cells, which normally bind with hormones such as testosterone.
Although tumour cells may initially respond to these therapies, most eventually develop resistance that causes prostate cancer cells to grow and spread, the researchers noted in the paper published in the journal OncoTargets and Therapy.
Anti-hormone therapies, or chemical castration, also may be used in the fight against prostate cancer.
“Cholesterol also can contribute to the development of anti-hormone resistance because cholesterol is converted into hormones in tumour cells; therefore, these cholesterol-forming pathways are attractive therapeutic targets for the treatment of prostate cancer,” Hyder explained.
Using a compound developed for the treatment of high cholesterol called RO 48-8071, the team administered the molecule to human prostate cancer cells.
They then tested the results in mice with human prostate cancer cells. Following injection of the compound, they found that the molecule was effective in reducing tumour growth.
IANS