Role of long non-coding RNAs and MYC interaction in cancer metastasis: A possible target for therapeutic intervention

The c-MYC is one of the most commonly discussed oncogenes in almost all cancers. c-MYC, as a proto-oncogene in normal cells, has found to be tightly controlled and regulated, both genetically and epigenetically. Evasion of the controlled checkpoint mechanisms during cancer causes a deregulated expression of c-MYC. Overexpression of c-MYC causes the onset of many hallmarks of cancer. Despite c-MYC being centrally located in several cancers, it is not feasible to target c-MYC in therapeutic resistant cancers. Similarly, long non-coding RNAs (lncRNAs) are deregulated during the genesis and progression of different cancers. LncRNAs contribute to almost 27% human genome and recent findings by tumor genome sequencing revealed many of the lncRNAs loci that are modified, deleted, amplified, and mutated during the different stages of cancer development. Recent studies also reported that multiple lncRNAs regulate c-MYC by different mechanisms and vice versa. Thus, oncogenic lncRNAs and c-MYC interaction are positioned to provide an interesting choice for therapeutic interventions in cancers. In this mini-review, we summarize the recent discoveries and explain how the interaction between oncogenic lncRNAs and c-MYC could be used as a possible target for therapeutic intervention in cancers, especially the therapeutic resistant metastatic cancers.