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Long non-coding RNA HOTAIR promotes UVB-induced apoptosis and in flammatory injury by up-regulation of PKR in keratinocytes

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Academic year: 2019

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Figure 3C), inhibited Bcl-2 expression (P o 0.01; Figure 3D), altered apoptosis-associated factors (Figure 3E), and increased the expressions of TNF-a (P o 0.05; Figure 3F and H) and IL-6 (P o 0.05; Figure 3G and H) compared with the pcDNA3.1 group in UVB-
Figure 5E) and decreased apoptosis (P o 0.05; Figure 5F and G), compared with sh-NC in UVB-treated cells.
Figure 6. Effect of HOTAIR and PKR on UVB-induced cell injury; A, Cell viability assay demonstrated overexpression of HOTAIR promoted UVB-induced cell viability inhibition by upregulation of PKR, and suppression of PKR reversed the results; B, Apoptosis as
Figure 7. Western blotting analysis of PKR on PI3K/AKT and NF-kB signaling pathways, which suggested that overexpression of PKR activated A, PI3K/AKT pathway and B, NF-kB pathway

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