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Main Category: Colorectal Cancer
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Article Date: 15 Aug 2013 - 5:00 PDT Current ratings for:
Colorectal cancer may be triggered by mouth bacteria
Two new studies published this week suggest that a type of gut bacteria found in the mouth may trigger colorectal cancer by influencing the immune response and switching on cancer genes.
The researchers believe their findings may lead to more timely and improved ways of diagnosing, preventing, and treating colorectal cancer.
Our gut contains trillions of bacteria, vastly outnumbering our own cells. These microbe communities maintain our health by training our immune system and helping us digest food. But they can also trigger disease.
There is evidence that an imbalance between the "good" and the "bad" gut bacteria may promote colon cancer.
The two new studies, published in the August 14th online issue of the journalCell Host & Microbe, focus on a genus of bacteria called Fusobacteria, and the species F. nucleatum in particular.
Colorectal cancer is the second leading cause of death from cancer among Americans. Researchers have found Fusobacteria from the mouth are also abundant in tissues from colorectal cancer patients.
Our mouths contain millions of bacteria
But until this latest research, it was not clear whether these gut microbes actually trigger tumors, and if so, how they do it.
In the first study, the researchers found Fusobacteria in benign tumors that can become cancerous over time. This might suggest that they contribute to the early stages of tumor formation.
Then, in mice bred to have a human-like form of colorectal cancer, the team found the bacteria sped up tumor formation by summoning a type of immune cell called myeloid cells, which penetrate tumors and trigger inflammations that can lead to cancer.
Senior author Wendy Garrett, of the Harvard School of Public Health and the Dana-Farber Cancer Institute in the US, told the press:
"Fusobacteria may provide not only a new way to group or describe colon cancers but also, more importantly, a new perspective on how to target pathways to halt tumor growth and spread."
In the second study, another team found that Fusobacteria use a molecule that lives on the surface of the bacterial cell to stick to and then invade human colorectal cancer cells.
The molecule, called Fusobacterium adhesin A (FadA), switches on genes that spur cancer growth, triggers inflammation in the human cancer cells, and spurs tumor formation.
The team also found that tissue from healthy individuals had much lower levels of FadA than tissue from patients with benign and cancerous colorectal tumors.
Plus, they identified a compound that can stop the effects of FadA on cancer cells.
Senior author Yiping Han, of Case Western Reserve University School of Dental Medicine in the US, said:
"We showed that FadA is a marker that can be used for the early diagnosis of colorectal cancer and identified potential therapeutic targets to treat or prevent this common and debilitating disease."
In another study of mice published earlier this year, researchers identified the mechanisms that help the good gut bacteria and the immune system to coexist. A group of immune cells called innate lymphoid cells (ILCs) seem to instruct the immune T cells to trust - that is, ignore - friendly gut bacteria, thereby allowing the immune system to maintain a friendly truce with these foreign entities.
Written by Catharine Paddock PhDCopyright: Medical News Today
Not to be reproduced without permission of Medical News Today Visit our colorectal cancer section for the latest news on this subject.
"Fusobacterium nucleatum Potentiates Intestinal Tumorigenesis and Modulates the Tumor-Immune Microenvironment"; Aleksandar D. Kostic, Eunyoung Chun, Lauren Robertson, Jonathan N. Glickman, Carey Ann Gallini, Monia Michaud, Thomas E. Clancy, Daniel C. Chung, Paul Lochhead, Georgina L. Hold, and others; Cell Host & Microbe 14(2) pp. 207 - 215 published online 14 August 2013; DOI: 10.1016/j.chom.2013.07.007; Link to Abstract.
"Fusobacterium nucleatum Promotes Colorectal Carcinogenesis by Modulating E-Cadherin/ß-Catenin Signaling via its FadA Adhesin"; Mara Roxana Rubinstein, Xiaowei Wang, Wendy Liu, Yujun Hao, Guifang Cai, Yiping W. Han; Cell Host & Microbe 14(2) pp. 195 - 206 published online 14 August 2013; DOI: 10.1016/j.chom.2013.07.012; Link to Abstract.
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posted by George B on 15 Aug 2013 at 7:15 am
"Plus, they identified a compound that can stop the effects of FadA on cancer cells."
What compound?!?
Editor's note:: Many thanks for your enquiry asking which compound stops the effect of FadA on cancer cells.
If you follow the link to the scientific report on the second study, which is included in the References tab at the bottom of our article, you will see the Abstract in Cell & Host Microbe where the researchers summarize what they did to find the compound and how they tested it:
"... FadA binds to E-cadherin, activates ß-catenin signaling, and differentially regulates the inflammatory and oncogenic responses. The FadA-binding site on E-cadherin is mapped to an 11-amino-acid region. A synthetic peptide derived from this region of E-cadherin abolishes FadA-induced CRC cell growth and oncogenic and inflammatory responses ..."
E-cadherin is a molecule that helps cells stick to each other and is important for maintaining tissue architecture. So the compound they found is a synthetic version of the part of E-cadherin that FadA binds to.
We hope this answers your query.
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