The research article describing this work entitled Differential Expression of Mimecan and Thioredoxin Domain-Containing Protein 5 in Colorectal Adenoma and Cancer: A Proteomic Study will be featured in the October 2007 issue of Experimental Biology and Medicine.

Adenoma is the major precursor lesion of colorectal cancer, one of the most common cancers worldwide. The elucidation of the molecular mechanism underlying adenoma is essential for early detection, prevention and intervention of colorectal cancer.

The research team, led by Maode Lai, a professor of molecular pathology, found 27 differentially expressed proteins in colorectal adenoma using two dimensional electrophoresis (2-DE) and mass spectrometry. Western-blot analysis clearly validated 2 differentially expressed proteins, mimecan downregulation and TXNDC5 upregulation in colorectal adenomas and cancers.

Adenoma is a very important step in the development of cancer. Discovering the biomarker of adenoma will improve the early detection and prevention of cancer, said Lai. 2-DE is an efficient traditional approach for the identification of differentially expressed proteins in cancer biology. Using this technology, we first identified 27 differentially expressed proteins in individual-matched colorectal normal, adenoma and cancer tissues.

This study found two novel proteins which have never been found to be associated with colorectal cancer. We clearly demonstrated that absence of mimecan and up-regulation of TXNDC5 were involved in the early development of colorectal cancer, said the article's first author Yinghong Wang. Our further work showed that mimecan can inhibit cell growth and induce cell apoptosis in colorectal cancer cells implying a candidate role as a tumor suppressor gene for the mimecan gene. These results suggested that mimecan might serve as a potential biomarker for future gene therapy.

Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, said Lai and his colleagues have performed a protein profiling proteomic study to understand the molecular mechanisms leading to colorectal cancer. It is this type of approach which can lead to the identification of biomarkers for the early detection of colorectal cancer, and targets for future gene therapy.

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Researchers found that when there are too many cheaters, the whole population pays the price. At that point, the study discovered, the cheaters have compensatory genetic mechanisms to recognize the problem, and some of them go back to cooperative behaviors that favor survival of the group “ and themselves.

The bacterium the scientists studied is important by itself “ it's an opportunistic pathogen that can cause persistent infections in humans, including pneumonia, and is often the cause of death for patients with cystic fibrosis, a chronic lung disease. It's also a serious concern with hospital-acquired infections, AIDS patients, people who use catheters, and other issues. The mutant cheating bacteria are often found in patients with these disease problems. Their emergence had appeared to be a paradox, however, because bacterial communication is required for infection.

This study resolved that paradox, suggesting that the emergence of a cheating sub-population is in fact favored when bacterial communication is required for survival. And it supports an unconventional approach to antibiotic therapy - interfering with bacterial communication. Such drug design concepts could become a new concept in antibiotics, researchers say.

The study also provides fundamental insights into the evolution of the quorum sensing mechanism among bacteria, why it's essential to group survival under certain conditions, and how some cheating bacteria can thrive without the ability to communicate.

Bacteria are very useful model organisms to study the process of evolution, researchers say, because of their fast growth. Unlike with higher organisms, their evolution can be observed in real time in the laboratory.

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