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. 2021 Jun 7;17(1):170–177. doi: 10.4103/1673-5374.314314

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Copyright: © Neural Regeneration Research

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6-OHDA-induced lincRNA-p21 upregulation targets TGIF1 by STAU1-mediated mRNA decay.

(A) The predicted lincRNA-p21 binding site within TGIF13′-untranslated regions. (B) Reverse transcription quantitative polymerase chain reaction analysis of TGIF1 mRNA levels in SH-SY5Y cells transfected with lincRNA-p21 siRNA and treated with 6-OHDA for 24 hours; GAPDH served as the internal control. (C) Interaction of TGIF1 mRNA with STAU1 was detected using the RNA immunoprecipitation assay in SH-SY5Y cells transfected with lincRNA-p21 siRNA. (D) Reverse transcription quantitative polymerase chain reaction analysis of STAU1 mRNA levels in SH-SY5Y cells transfected with STAU1 siRNA for 24 hours. The data are shown as the mean ± SD (n = 5); &&P < 0.01, vs. NC group (Student’s t-test). (E) Reverse transcription quantitative polymerase chain reaction analysis of TGIF1 mRNA levels in SH-SY5Y cells transfected with STAU1 siRNA and treated with 6-OHDA for 24 hours. (F) Representative western blot and quantification data of TGIF1 in SH-SY5Y cells transfected with lincRNA-p21 siRNA or STAU1 siRNA, and treated with 6-OHDA for 24 hours. The data are shown as the mean ± SD (n = 5; one-way analysis of variance followed by Bonferroni post hoc test). &&P < 0.01, vs. NC siRNA group; #P < 0.05, ##P < 0.01, vs. 6-OHDA treatment group. 6-OHDA: 6-Hydroxydopamine; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; siRNA: small interfering RNA; STAU1: double-stranded RNA-binding protein Staufen homolog 1; TGIF1: TG-interacting factor 1. Con: Control; NC; negative control.