Over the past few years, researchers have discovered that naturally-occurring molecular snippets called "microRNAs" influence normal human growth and development. In 2005, Greg Hannon, Scott Lowe, Scott Powers, together with Scott Hammond at UNC, showed that a cluster of microRNAs - referred to as the "mir-17-92 cluster" - is overexpressed in certain human tumors and can promote tumorigenesis in mice.
A segment of human chromosome 13 containing mir-17-92 is known to be "amplified" or present in excess copies in several tumor types, and the five microRNAs encoded by this DNA segment are present at abnormally high levels in human B-cell lymphoma cell lines as well as in biopsies of human lymphomas and colorectal carcinomas. To test whether increased levels of the microRNAs could indeed contribute to cancer, mouse cells were engineered with high levels of the microRNAs. When the microRNAs were overexpressed, tumor development was accelerated in a mouse model of B-cell lymphoma and survival rates decreased.
Moreover, lymphomas engineered to have high levels of the microRNAs consistently invaded organs including liver, lung, and kidney and lacked the extensive "programmed cell death" which otherwise keeps tumors in check. The observations identify the first that non-coding RNAs causally contribute to tumor development and as such provide insights into a completely novel mechanism of cancer development.
