TUG1 promotes retinoblastoma progression by sponging miR-516b-5p to upregulate H6PD expression

BACKGROUND: Retinoblastoma (RB), depicted as an aggressive eye cancer, mainly occurs in infancy and childhood and is followed by high mortality and poor prognosis. Increasing evidence has revealed that long noncoding RNA taurine upregulated gene 1 (TUG1) is closely linked to the progression of diverse cancers. Nonetheless, the specific function and molecular regulatory mechanism of TUG1 in RB still need to be explored. METHODS: To explore the specific role of TUG1 in RB. TUG1 expression was detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell counting kit-8 (CCK-8), colony formation, 5-ethynyl-2’-deoxyuridine (EdU), caspase-3, terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) and western blot assays were utilized to study the role of TUG1 in RB. The binding relation between miR-516b-5p and TUG1 or hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase (H6PD) was analyzed by luciferase reporter and RNA immunoprecipitation (RIP) assays. RESULTS: The expression of TUG1 was upregulated in RB cells. TUG1 knockdown repressed proliferation ability and promoted apoptosis ability of RB cells. Moreover, TUG1 could bind with miR-516b-5p, which targeted H6PD in RB. In addition, the expression of H6PD was negatively and positively regulated by miR-516b-5p and TUG1 in RB, respectively. Finally, H6PD overexpression could partially offset the effects of TUG1 deficiency on cell proliferation and apoptosis. CONCLUSIONS: TUG1 promoted the development of RB by sponging miR-516b-5p to upregulate H6PD expression, which might provide a new thought for researching RB-related molecular mechanism.