Cell Death and Disease · 2020 · 96 citations · 39 references
Life SciencesMolecular BiologyOncologyCarcinogenesisGene ExpressionMolecular OncologyCancer TranscriptomicsNoncoding Rna BiologyNoncoding Rna In CancerNoncoding Rna TranscriptomicsRna-binding ProteinsRna-protein InteractionsCell StiffnessCell Stiffness RegulationEpithelial-mesenchymal Transition MarkersLong Non-coding Ribonucleic AcidsLong Noncoding Rna RegulationLung AdenocarcinomaStiffnessTnm Staging System
There is increasing evidence that long non-coding RNAs (lncRNAs) play important roles in human tumorigenesis. By using publicly available expression profiling data from lung adenocarcinoma and integrating bioinformatics analysis, we screened a lncRNA, LINC00472. LINC00472 expression in lung adenocarcinoma tissues was significantly lower and tightly associated with patient prognosis and TNM clinical stages in lung adenocarcinoma. LINC00472 also inhibited lung adenocarcinoma cell migration and invasion and increased cell stiffness and adhesion. RNA pull down and RIP assays identified that LINC00472 interacted with the transcription factor Y-box binding protein 1 (YBX1), which partially reversed the inhibition of cell migration and invasion and increased LINC00472-induced cell stiffness and adhesion. LINC00472 also regulated the density and integrity of F-actin in A549 and PC-9 cells possibly via YBX1. LINC00472 inhibited the cell epithelial-mesenchymal transition (EMT) processes via the modulation of YBX1. These results indicated that LINC00472 inhibited the cell EMT process by binding to YBX1, and affected the mechanical properties of the cell, ultimately inhibited its ability to invade and metastasize. Collectively, the present study provides the first evidence that LINC00472 changes the mechanical properties and inhibits the invasion and metastasis of lung adenocarcinoma cells.
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