Oral Bacteria and Colorectal Cancer

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How Oral Bacteria Make Malignant Colorectal Cancer Progress Aggressively

Scientists have identified a molecular mechanism through which an oral bacterium accelerates colorectal cancer growth. Experts always suspected that there was a molecular mechanism that hastened colorectal cancer’s progression.

Until recently, it wasn’t clear why a third of the patients diagnosed with colorectal cancer also presented more aggressive symptoms than their counterparts. Intense testing has now shown detection of Fusobacterium nucleatum bacteria in such patients.

The conclusions of the study were published in a paper in the journal EMBO Reports, indicating that the Fusobacterium nucleatum microorganism tends to advance the growth of cancerous cells while not affecting non-cancerous cells.

According to the researchers involved in the study from Columbia University, the findings act as evidence that some colorectal cancers develop more aggressively than others. The study’s senior author Prof. Yiping W. Han—a professor of microbial sciences in the university’s College of Dental Medicine­—and her team members also claim that they have singled out a protein that could not only make testing for more aggressive cancers simpler but also pave the way for treatment for colorectal and other cancers.

How Does Colorectal Cancer Develop?

The statistics from the American Cancer Society paint a grim picture of how around 1 in 24 women and 1 in 22 men in the United States will get diagnosed with colorectal cancer in the course of their lives.

Moreover, startling figures from 2016 show that about 1.5 million people had colorectal cancer in the US, and only some of these patients are cancer-free.

Colorectal cancer presents itself in the colon or the rectum of the patient. The colon and rectum are the final sections of the digestive GI (gastrointestinal) tract. Cancer develops when healthy cells grow uncontrollably, or the abnormal cells survive the onslaught of your body’s defense mechanism.

When we eat or drink anything, it gets digested and assimilated. Most of the food gets digested when it passes through the stomach and the small intestine, but the colon absorbs water and nutrients from the remaining assimilated food. All this waste then collects in the rectum where it gets stored until it’s ready for expulsion through the anus.

Polyps or growths in the mucosa, which is the tissue that forms the lining of the colon and rectum, are the most common pre-cancerous indication of colorectal cancer. They develop very slowly; as long as 20 years in some instances.

The most common polyps are the adenomatous polyps or adenomas. These grow from the glands that produce the cells that make the lubricating epithelial mucosal lining in the colon and rectum.

About 30-50 percent of people will, at some point, develop at least one Adenoma, which can become cancerous in most instances. Fortunately, less than 10 percent of known diagnosed cases progress invasively.

The Role Of Oral Bacterium In Colorectal Cancer

Scientists already know that abnormal cell growth leads to cancerous adenomas in colorectal cancer. These abnormal cells build up over time due to genetic mutations.

More recent discoveries increasingly show the presence of the oral F. nucleatum bacterium, which mostly shows up in periodontal diseases. According to Prof. Han, these bacteria may play a significant role in colorectal cancer’s progression. “Mutations are just part of the story. Other factors, including microbes, can also play a role,” said Prof. Han, reported Medical News Today.

Previously, Prof. Han and team had observed how the F. nucleatum produced the FadA adhesin molecule. Scientists already knew how this molecule triggered a series of molecular events in the colon, which ultimately leads to several cancers.

Additionally, they also observed how the protein only affected the cancerous cells in the colon and rectum while leaving the healthy cells unharmed.

Why Does The Bacterium Only Affect Cancerous Cells

Prof. Han says that her primary intention behind conducting the recent study was to establish a credible link between F. nucleatum and why it only affects cancerous cells.

The research team examined non-cancerous colon cell cultures and found that they didn’t produce any Annexin A1 protein, which causes cancer cell growth. Further testing revealed how blocking the Annexin A1 protein in cell cultures and mice inhibited the F. nucleatum from attaching to cancer cells, thereby stopping the aggressive cell growth.

A few more tests revealed the insidious feedback loop of how F. nucleatum caused excessive cancer cell growth, which leads to more Annexin A1 being produced, which attracted more F. nucleatum. The loop repeats itself, and the patient reels from an aggressive cancer prognosis.

The study does offer a silver lining by proposing what they term as the two-hit model, which firstly targets the genetic mutations and then targets the cancer accelerant bacteria F. nucleatum. “We propose a two-hit model, where genetic mutations are the first hit. F. nucleatum serves as the second hit, accelerating the cancer signaling pathway and speeding tumor growth,” concluded the study.

The research team scoured through the national cancer records database and found 466 people who matched the molecular details of their focus group. Upon analyzing the records, the researchers noted that patients with higher levels of Annexin A1 had more aggressive colorectal cancer irrespective of age, gender, cancer stage, and grade.

The research team now plans to figure out how to use the Annexin A1 protein as an aggressive colorectal cancer identifying marker. If they succeed, it may lead to targeted colorectal cancer treatments.



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