Researchers from the University of Minnesota have published an article titled “Sequential expression of miR-182 and miR-503 cooperatively targets FBXW7, contributing to the malignant transformation of colon adenoma to adenocarcinoma” in the Journal of Pathology, where they identified microRNAs (miRNAs) responsible for the cancerous progression of colon polyps.
These new data can allow physicians to provide more specialized and earlier treatment that could prevent colon cancer development.
“With the advanced screenings we now have available, why are so many people still being diagnosed with colon cancer? We really wanted to understand if there was a way to stop the disease before it starts, before benign polyps became cancerous tumors,” lead author of the study Subbaya Subramanian, Ph.D., assistant professor in the Division of Basic and Translational Research in the Department of Surgery in the University of Minnesota Medical School and member of the Masonic Cancer Center, University of Minnesota said in a University press release.
To better understand the role of miRNA dysregulation in cancer progression, the research team analyzed miRNAs present in colon polyps, finding that miR-182 and miR-503 promote the progression of colon adenoma to adenocarcinoma by synergistically down-regulating a specific tumour suppressor factor.
Moreover, upon introducing miR-503 into a cell line derived from a benign adenoma, the scientists could observe this microRNA conferred tumourigenic potential to the benign cells. Also, if both miR-182 and miR-503 were blocked in colon cancer cell lines, the capacity of these tumors to proliferate and develop was severely impaired.
To confirm their laboratory results, the team examined the levels of miR-182 and miR-503 in more than 200 colon cancer patients with 12 year survival outcome data, showing that elevated levels of both miRNAs was associated with decreased patient survival, transforming these two molecules into possible colon cancer biomarkers.
According to the authors, future studies should aim towards the development of drugs that can be used in the clinic to specifically target miR-182 and miR-503.