is the most frequently mutated gene in human cancers. Most genomic alterations are missense mutations, which cause a loss of its tumour suppressor functions while providing mutant p53 (mut_p53) with oncogenic features (gain-of-function). Loss of p53 tumour suppressor functions alters the transcription of both protein-coding and non-protein-coding genes. Gain-of-function of mut_p53 triggers modification in gene expression as well; however, the impact of mut_p53 on the transcription of the non-protein-coding genes and whether these non-protein-coding genes affect oncogenic properties of cancer cell lines are not fully explored. In this study, we suggested that (also known as ) is a long non-coding RNA regulated by mut_p53 and proved that mut_p53 directly regulates by binding to an enhancer region downstream of the locus. We also showed that the loss or downregulation of impairs cell migration in a breast cancer cell line. Eventually, by performing a combined analysis of RNA-seq data generated in -silenced and knockout cells, we showed that and mut_p53 share common gene pathways. Overall, our findings underline the importance of ncRNAs in the mut_p53 network in breast and ovarian cancer cell lines and in particular the importance of in mut_p53 pro-migratory pathways.