A recent advance in transcriptomics has spawned the ‘Decade of non-coding RNAs’ by potentiating the growing numbers of long non-coding RNA in cancer. LncRNA involvement in cancer denotes its significance beyond our perception as they participate in tumor suppression and promoting oncogenesis, which raises them as a mighty class of effectors or regulators. Aberrantly expressed lncRNAs interact with major protein and coding partners, which ultimately deregulate normal cellular processes and drive the cell towards malignant state. Identification of theses interactions are utmost important as lncRNAs can be ideal targets for therapy. Dysregulation of lncRNAs by genomic alterations like single nucleotide variations and gene fusions are also potential modulators of their secondary structure. In this review, the authors discuss the various molecular interactions of lncRNAs with major bio-molecules and genetic variations in lncRNA genes and their importance in cancer. This systematic review outlines the vivid role of lncRNAs in cancer context and opens up future conceptual applications.
Long non-coding RNAs as major hallmarks and enabling cancer characteristics. (In clockwise direction) PCAT1 is a prime lncRNA involved in increased transcription of cMYC exerting constitutive cell proliferative signals. ANRIL can potentially regulate the INK4b-ARF-INK4a locus to a diminished p15, p16 and p14 activity. TERRA acts as an RNA primer in the TERT mediated telomere end promoting replicative immortality. The EMT modulators ZEB1& ZEB2 were found to be upregulated by an overexpressed lncRNA-ATB favoring invasion. The low levels of ncRuPAR is linked to increased VEGF mediated angiogenesis. Expression of apoptosis inducing TNFSF10 is suppressed by an active SOCS2-AS. An energetics reprogramming mechanism by blocking glucose uptake is exhibited by lncRNA-MIF. The transcriptional signal of immune responsive gene is controlled by lincRNA COX2 getting detrimental on immunity based tumor destructive program. DDSR1 is involved in preventing the assembly of BRCA2/RAP80/hnRNPUL1 causing a non-responsiveness to DNA damage increasing genomic instability. The inflammatory cells are known to promote tumor through IL-1b/MMP signaling and HOTAIR is linked to inhibit IL-1b