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In a study of mice, scientists from the University of California, Los Angeles (UCLA), David Geffen School of Medicine found that raising cholesterol levels in animals caused intestinal stem cells to divide faster, increasing tumor formation by 100 times. This study identified a molecular pathway that could serve as a new drug target for colon cancer treatment.
Although the link between dietary cholesterol and colon cancer has been established for some time, no one had previously explained the biological mechanism behind it. This study provides that explanation for the first time, offering a clearer picture of how diet can directly drive cancer development at the cellular level.
Scientists increased cholesterol in some intestinal stem cells of mice by introducing more cholesterol-rich substances into their diet. In a parallel experiment, researchers altered a gene that regulates phospholipids — the main type of fat found in cell membranes — prompting the cells to produce more cholesterol on their own.
In both groups, stem cells showed increased reproductive capacity. As cholesterol levels rose, cells divided more rapidly, causing the intestines to grow longer. These changes significantly accelerated the rate of tumor formation in the colon. The findings point to a clear molecular pathway through which excess cholesterol fuels colon cancer growth, and one that researchers now hope to target with new drug therapies.
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About Sai Sree
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