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. 2018 Oct 19;9(11):1068. doi: 10.1038/s41419-018-1088-6

Fig. 5. Amplified miR4673 signalling coerces transcriptional fingerprint of SKBR3 cells into a G0 signature.

Fig. 5

a The short isoform of cyclin-D1 only encodes for retinoblastoma binding domain. The short isoform of catenin-β1 only encodes for the phosphorylation domain of the protein. The graphs show altered molecular fingerprint of SKBR3 cells following the amplification of endogenous miR4673 signalling (* indicates p < 0.05, ** indicates p < 0.01). E1 and E2 are sequential electroporations 24 h apart. We used two separate sets of primers to fingerprint the 5ˊ and 3ˊ notch-1 locus. b Schematic demonstration of system-level miR4673 interactions that improve fitness profile of neoplastic cells. Interactions triggered by the miRNA signalling eventually improve anti-oxidant defence capacity and accelerate DNA repair mechanisms through non-homologous end-joining. c Schematic representation of cell cycle shows prolonged G0 subsequent to the amplification of the endogenous miRNA activity that instructs inhibition of G1/S and G2/M cycle checkpoints simultaneously