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. 2020 Feb 18;21(4):1941–1949. doi: 10.3892/mmr.2020.10989

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Copyright: © Liu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 5. — TET2 regulates the expression levels of proinflammatory cytokines at the mRNA and protein level in HaCaT cells. RT-qPCR was performed to determine the mRNA expression levels of (A) LCN2, (B) S100A7, (C) MMP9, (D) CXCL1, (E) IRF7 and (F) IL7R following TET2 knockdown in HaCaT cells. RT-qPCR was performed to determine the mRNA expression levels of (G) LCN2, (H) S100A7, (I) MMP9, (J) CXCL1, (K) IRF7 and (L) IL7R following TET2 overexpression in HaCaT cells. Protein levels of proinflammatory cytokines were (M) determined by western blotting and (N) quantified following TET2 knockdown in HaCaT cells. Data are presented as the mean ± SD of three independent experiments performed in triplicate. *P<0.05, **P<0.01, ***P<0.001 vs. NC group. TET2, ten-eleven transloation-2; RT-qPCR, reverse transcription-quantitative PCR; LCN2, lipocalin 2; S100A7, S100 calcium binding protein A7; MMP9, matrix metallopeptidase 9; CXCL1, C-X-C motif chemokine ligand 1; IRF7, interferon regulatory factor 7; IL7R, interleukin-7 receptor; NC, negative control; si, small interfering RNA.