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A group of researchers from the University of California, Riverside found out that sustaining a sense of balance of proteins found in the colon could help diminished the threat of developing colon cancer and colitis.

According to Science News Line, the researchers led by cell biologist Professor Frances M. Sladekused two major isoforms which stemmed from hepatocyte nuclear factor 4-alpha or HNF4-alpha that has long been present in mice: P1-HNF4-alpha and P2-HNF4-alpha

"P1 and P2 have been conserved between mice and humans for 70 million years. Both isoforms are important and we want to keep an appropriate balance between them in our gut by avoiding foods that would disrupt this balance and consuming foods that help preserve it. What these foods are is our next focus in the lab,"Sladek pointed it out.

The study benefitted beforehand from the researchers' familiarity in the field of cell biology thatHNF4-alpha is a transcription factor which is a work house protein for the cell.

HNF4-alpha takes the part of setting down DNA into RNA which is then converted to another set of proteins as mentioned and does the work for the cell. Sladek and her team have publicizedthat these isoforms accomplishtasks in the intestine that are not superfluous and prove to beof great importance to colitis and colitis-associated colon cancer.

Of all the adult tissues located in the body, the intestine which is a portion of the alimentary canal is the only one which vents out both P1 and P2.

In the said experiment, mice which were engineered to only either possess P1 or P2 were laid open to both a carcinogen and an irritant to pressure the colon which is lined with epithelial cells.

They found out that the P1 mice presented a fewer growth of abnormal tissues than the wild type control subject and were resilient to colitis after being subjected to an irritant.

It differed greatly with the P2 mice as it displayed an abundance of tumor growth and was non-resistant to colitis.

Afterward, they then surveyed both mice with regards to their genes. Again, the P2 mice showed more consequence for colitis as a greater number of RELM-beta was found in the G.I. tract.

"This makes sense since a reduced barrier function means bacteria can go across the barrier, which activates RELM-beta. We also found that the P2 protein transcribes RELM-beta more effectively than the P1 protein," Sladek said.