Abstract

Taurine-upregulated gene 1 (TUG1) is a long noncoding RNA (lncRNA) that has previously been linked to the development and progression of several cancer types. Its expression and mechanistic role in retinoblastoma (RB), however, remains to be established. Herein, we found that RB tissue samples exhibited TUG1 upregulation. RB cell lines similarly exhibited marked TUG1 upregulation. Real-time cellular analysis (RTCA) and colony formation assays were then used to gauge RB cell proliferation, while transwell assays were conducted to assess the metastatic and invasive potential of these cells. In these assays, TUG1 upregulation was found to promote RB cell proliferative, migratory, and invasive activity while inducing the epithelial–mesenchymal transition (EMT). Subsequent quantitative real-time polymerase chain reaction (qPCR) and Western blotting indicated that this lncRNA functions at least in part by influencing the expression of Notch signaling pathway genes, which were downregulated following TUG1 knockdown in RB cells. Together, these data suggested that TUG1 can promote RB cell malignancy via the Notch signaling and EMT pathways, contributing to negative patient outcomes.

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