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. 2021 Jan 15;12(1):86. doi: 10.1038/s41419-020-03305-z

Fig. 4. MiR-330 directly binds to SPRR2C, STAT1, and S100A7.

Fig. 4

A HaCaT cells were starved in serum-free DMEM for 24 h, treated with IL-22 (100 ng/ml) in serum-free DMEM for another 24 h or not treated, and then examined for the expression of miR-330 by real-time PCR. B The expression of miR-330 was determined in 12 psoriatic lesions and 12 nonlesion tissues by real-time PCR. C The protein content and distribution of STAT1 and S100A7 in the psoriatic lesion and nonlesion tissue samples were determined by immunohistochemistry (IHC) staining. D The protein levels of STAT1 and S100A7 in the psoriatic lesion and nonlesion tissue samples were determined by immunoblotting. E HaCaT cells were treated with IL-22 and examined for the protein levels of STAT1 and S100A7 by immunoblotting. F SPRR2C knockdown or overexpression was achieved in HaCaT cells by the transfection of si-SPRR2C or SPRR2C-overexpressing vector; the transfection efficiency was confirmed by real-time PCR. G HaCaT cells were transfected with si-SPRR2C or SPRR2C-overexpressing vector and examined for the protein levels of STAT1 and S100A7 by immunoblotting. H MiR-330 overexpression or inhibition was achieved by the transfection of miR-330 or antagomir-330-5p; the transfection efficiency was confirmed by real-time PCR. I HaCaT cells were transfected with miR-330 or antagomir-330-5p and examined for the protein levels of STAT1 and S100A7 by immunoblotting. J, K Wild-type and mutant-type SPRR2C, STAT1 3′UTR, and S100A7 3′UTR luciferase reporter vectors were constructed as described in “Materials and Methods”. These vectors were cotransfected into 293T cells with miR-330 or antagomir-330-5p, and the luciferase activity was determined. **P < 0.01, #P < 0.05, ##P < 0.01.