This anti-cholesterol drug might slow down colorectal cancer: Study
What's the story
Statins, a class of drugs commonly used to lower cholesterol levels, have shown promise in slowing down the growth of colorectal tumors. The discovery was made by researchers from Shiv Nadar University and the Indian Institute of Science Education and Research (IISER) Pune. Their study suggests that these widely-used medications could be repurposed for cancer treatment. However, further clinical trials are needed to validate these findings before statins can be integrated into standard cancer therapies.
Repurposing benefits
Drug repurposing in cancer treatment
The concept of drug repurposing, which involves finding new uses for existing medications, is gaining traction in the fight against diseases like cancer. This strategy is particularly appealing as it can significantly reduce the cost and time involved in developing new drugs from scratch. The rise of computing power, artificial intelligence, and bioinformatics has made it easier to identify potential new uses for existing drugs.
Mechanism
Cholesterol metabolism linked to colorectal cancer
Sanjeev Galande, the study's senior author and dean of the School of Natural Sciences at Shiv Nadar University, explained that cholesterol metabolism is linked to colorectal cancer. He said, "While certain cancers have shown signs of slowing down due to the use of statins, the precise and specific mode of action of the drugs has not been demonstrated yet."
Study findings
Statins halt cancer growth
The research team demonstrated that statins can halt cancer growth at the molecular level through cell culture and mouse experiments. When colorectal cancer cells were treated with statins in the lab, they showed tumor-suppressing behavior. The study concluded, "Our findings strongly suggest that statins effectively mitigate the progression of colorectal tumors both in cultured (colorectal cancer) cells and in mice."
Pathway targeting
Molecules target specific pathways
The research also found that statin molecules specifically targeted the 'Wnt/b-catenin' signaling pathway, which is critical to the formation of colorectal cancer adenoma. This was seen through a reduction in the action of SATB1, a protein that promotes tumor growth, and an increase in SATB2, which suppresses it. The change in gene activity halted cancer cell growth in lab models mimicking tumors closely.