Ignoring inflammation in the gut can lead to colon cancer

You may ignore the inflammation in your gut from time to time but by doing so, you increase your colon cancer risk by 500 per cent.

Sounds scary, right? But that's exactly what the revelations of a study suggest.

Through the study, researchers identied, an indicator in the physical and chemical components of a cell that could not only serve as an early warning of colon cancer but potentially be harnessed to counteract advanced forms of the disease.

"A quarter of the world's population is affected by some type of gut inflammation and these patients always have a much higher chance of developing colon cancer," said lead author Xiling Shen, associate professor at Duke University in North Carolina, US.

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The scientists focused on a microRNA--a class of naturally occurring, small non-coding ribonucleic acid (RNA) molecules--called miR-34a that gives cancer stem cells the odd ability to divide asymmetrically. This process controls the cancerous stem cell population and generates a diverse set of cells.

However, the problem showed up when the mice's tissues became inflamed. Without any microRNA miR-34a, their stem cells quickly grew out of control and formed many tumour-like structures, the researchers elucidated. Triggered to act when the gut becomes inflamed, miR-34a forces the process of asymmetrical division, helping to control normal stem cell populations, the findings, published online in the journal Cell Stem Cell, revealed.

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Even in the early stages of tumour growth, the microRNA remains active to keep the cancer stem cell population down. As the cancer progresses however, its cells develop mutations that enable shutting off miR-34a, causing cells to divide into flexible hybrids that can revert back into stem cells if needed. It's this flexibility that makes late-stage cancers so difficult to eradicate, the researchers explained.

Colon cancer development is intricately linked to a specific microRNA that dictates how cells divide, the study said.

(With IANS inputs)