Interestingly, overexpression of LINC00665 depleted the expression of MTF1 at both the mRNA and protein levels, whereas knockdown of STAU1 significantly increased MTF1 expression and could partially rescue the LINC00665-induced reduction of MTF1 levels (Figures 3A and 3B). To explore the mechanism of this LINC00665/MTF1 axis, an RNA-IP assay was used to verify the association among LINC00665, MTF1, and STAU1. The relative enrichment levels of LINC00665 and MTF1 were both significantly increased in the anti-STAU1 group compared to those in the anti-IgG group (Figure 3C). Furthermore, luciferase gene reporter assays were performed to clarify the association between LINC00665 and the MTF1 3′ UTR, and to identify the SBS. As shown in Figure 3D, the relative luciferase activity in the MTF1-3′ UTR-wild-type (WT) + LINC00665 group was significantly decreased compared with that in the NC group, whereas there was no such difference between the MTF1-3′ UTR-mutant-type (Mut) + LINC00665 and control groups. After treatment with actinomycin D, quantitative real-time PCR was used to compare the half-life of MTF1 mRNA in the two groups, showing a significantly shortened half-life in the LINC00665+
