Fig. 6: ZFP36L1 accelerated SDC4 mRNA degradation by binding to the ARE element. | Oncogene

Fig. 6: ZFP36L1 accelerated SDC4 mRNA degradation by binding to the ARE element.

From: Low expression of ZFP36L1 in osteosarcoma promotes lung metastasis by inhibiting the SDC4-TGF-β signaling feedback loop

Fig. 6: ZFP36L1 accelerated SDC4 mRNA degradation by binding to the ARE element.

mRNA stability assays (A) were performed to determine the stability of SDC4 mRNA that was regulated by ZFP36L1, and the half-life of SDC4 mRNA (B) was analyzed. RIP assays (C) and RNA pull-down assays (D) were carried out to confirm the binding relationship between ZFP36L1 and SDC4 mRNA. E Schematic representation of the predicted AREs in the 3’UTR of SDC4 mRNA (NM_002999.4) and construction of corresponding reporter plasmids. The 3’UTR in TNF mRNA (NM_000594.4) was used as a positive control. F Renilla luciferase activity assays were conducted to determine the role of AREs in the 3’UTR of SDC4 mRNA in the regulation of mRNA decay. RIP assays (G) and RNA pull-down assays (H) confirmed that ARE3 was the most important element for ZFP36L1 binding. I, J, RFP plasmids were constructed by fusing 3 AREs with RFP genes. mRNA stability assays (I) were performed to determine the function of AREs in regulating RFP mRNA decay, and the half-life of RFP mRNA (J) was calculated. The data are shown as means ± SEMs; *P < 0.05, **P < 0.01.

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