Might statins help fight colon cancer tumor growth?

• Colon cancer screening looks for the presence of polyps, some of which can become cancerous.
• One type, serrated adenoma, is considered pre-cancerous, can come back after it is removed and can lead to particularly invasive colon cancers.
• Researchers have discovered a mechanism that drives these cancers, which involves dysregulation of cholesterol metabolism, in a preclinical trial.
• This means there is the possibility this cholesterol dysregulation could be targeted by statins, and trials are planned to investigate this further.

Colon cancer is the third most prevalentTrusted Source type of cancer worldwide, and it can be screened for in order to catch it as early as possible.
Screening for colon cancer is done either through a fecal immunochemical test, which looks for blood in the stool that can come from polyps, or through a colonoscopy, to visualize the polyps.
There are two types of polypsTrusted Source:

• hyperplastic polyps that are typically benign
• adenomatous polyps (adenomas), which may turn into cancer.

Treatment generally involves removal of these polyps.

Challenges in treating colon cancer

One particular type of polyp, known as a serrated adenoma, is considered precancerous, and needs to be removed completely.
This poses a challenge as the polyps are flat, rather than growing on stalks like other polyps, and are harder to visualize due to this and the part of the colon they appear in.
Cancers from this type of polyp make up 15 to 30% of colorectal cancersTrusted Source, and they are often particularly invasive and resistant to treatments.
So far, it has been unclear exactly why this particular type of polyp was more likely to result in cancer than other types of polyps, but now, a metabolic mechanism has been proposed by a group of scientists from Weill Cornell Medicine, NY.
The results of their study appeared in in Nature Communications on December 13, 2023.

What does cholesterol have to do with colon cancer?

Previous research by some members of the team had shown that serrated adenoma polyps had lower levels of a protein kinase C (PKC) enzyme, which is responsible for regulating a number of genes involved in cell proliferation, among other cell metabolic pathways. The cells also evaded the body’s immune system, allowing the cancerous tumor to grow.’
In their latest study, the researchers used a previously developed mouse model that developed these serrated lesions in the colon.
The researchers started by analyzing the genes transcribed in these tumor cells, and found that cholesterol synthesis remained high in these cells, despite the high level of cholesterol present in them. This suggested cholesterol synthesis had become dysregulated in these tumor cells.
Further analysis of mouse tumor cells showed that loss of the protein kinases led to an activation of a transcription factor called SREBP2, which switches on cholesterol production.
Cholesterol is a driver of many metabolic processes, and the study authors showed that cholesterol drove cancer in these cells, initiating the growth of tumors.

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