In the past few years, scientists have achieved significant progresses in the study on the function of non-coding RNAs(IncRNAs). As the important regulatory factor, IncRNAs has been found to play important role in many disease progress including cancer. Researchers from Harvard Medical School have found that a subtype of IncRNA may promote the expression of BRAF and activation of MAPK to cause cancer. This study was published on Cell.

Over the past few years, remarkable progress has been made in establishing long non-coding RNAs as important regulators of various biological processes. Given their critical roles, it is not surprising that aberrant expression and/or function of IncRNAs are implicated in the development of diseases such as cancer.

Pseudogenes, a sub-class of IncRNA genes that developed from proteins, have long been viewed as non-functional genomic relicts of evolution. However, the vast majority of pseudogenes have protein-coding parental counterparts with which they share high sequence homology, which enables pseudogenes to participate in posttranscriptional regulation of their parental genes.

In this study, scientists report that mice engineered to overexpress either the full-length murine B-Raf pseudogene Braf-rs 1 or its pseudo “CDS” or “3′ UTR” develop an aggressive malignancy resembling human diffuse large B cell lymphoma. They show that Braf-rs 1 and its human ortholog, BRAFP1, elicit their oncogenic activity, at least in part, as competitive endogenous RNAs(ceRNAs) that elevate BRAF expression and MAPK activation in vitro and in vivo.

Their engineered mouse models demonstrate the oncogenic potential of pseudogenes and indicate that ceRNA-dediated microRNA sequestration may contribute to the development of cancer.

Reference:Karreth F A, Reschke M, Ruocco A, et al. The BRAF pseudogene functions as a competitive endogenous RNA and induces lymphoma in vivo[J]. Cell, 2015.