starBase was used to predict the existence of the binding site between LINC00665 and TAF15 (Figure S1B), and their interaction was confirmed with RNA immunoprecipitation (RNA-IP) and RNA pull-down assays. As shown in Figure 2B, the enrichment of LINC00665 was significantly higher in the anti-TAF15 group compared with that in the anti-immunoglobulin G (IgG) group. The RNA pull-down assay also revealed that TAF15 could bind to LINC00665 (Figure 2C). Therefore, we hypothesized that LINC00665 was involved in the TAF15-mediated regulation of glioma cells. In exploring the mechanism in this regulation network, we found no significant difference of the nascent LINC00665 expression level between the TAF15 overexpression group and the NC group (Figure 2D). However, the half-life of LINC00665 was found to be significantly prolonged in the TAF15+ group compared with that in the TAF15+-negative control (NC) group (Figure 2E). These results confirmed that LINC00665 stabilized by TAF15 could inhibit the malignant progression of glioma cells.
