Transposable elements (TEs) make up 46.7% of all nucleotide sequences in the human genome and include retroelements and DNA transposons. They are the evolutionary sources of many protein-coding genes; regulatory sequences; and noncoding RNAs (ncRNAs), including circular RNAs and microRNAs.

TEs induce genomic instability, promote recombination events, inactivate tumor suppressor genes, and activate oncogenes, thus facilitating carcinogenesis. In addition, TE transcripts can competitively interact with specific microRNAs that serve as targets for circular RNAs. The common origin of microRNAs and circular RNAs originating from TEs suggests the presence of complementary sequences. TE transcripts therefore act as competing endogenous RNAs (ceRNAs) for microRNAs to level their inhibitory effect on target mRNAs.

An analysis of the literature revealed 12 transposon-derived microRNAs that interact with circular RNAs during breast carcinogenesis. The review is the first to consider the interactions between several RNA classes (TEs, circular RNAs, and microRNAs with their target mRNAs) in the pathogenesis of breast cancer (BC).

This allows a new insight into the mechanisms of carcinogenesis in BC for the development of highly specific targeted drugs.