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. 2022 Jan 28;113(3):986–1001. doi: 10.1111/cas.15268

FIGURE 8.

FIGURE 8

miR‐181a‐5p inhibits serine/threonine kinase 16 (STK16) expression through directly targeting ETS1. (A) The predictive binding of miR‐181a‐5p and ETS1. (B) The luciferase activity of mutant or wild‐type ETS1 mRNA 3′UTR in H1975 cells transfected with miR‐181a‐5p mimic or inhibitor. (C, D) Expression of ETS1 in H1975 cells transfected with miR‐181a‐5p mimic or inhibitor. (E) Expression of ETS1 and STK16 in H1975 cells transfected with miR‐181a‐5p mimic and transduced with ETS1 expression vector. (F) ETS1 binding site (BS) in STK16 promoter schematic diagram. (G) Chromatin immunoprecipitation assay of ETS1 binding with STK16. (H, I) Pearson correlation scatter plots in lung adenocarcinoma (LUAD) tissues (n = 20). *P < .05, **P < .01, ***P < .001 compared with NC or IgG. ### P < .001 compared with miR‐181a‐5p mimic+Vector. (J) Schematic representation showing the mechanism that exosomes from M1‐polarized macrophages inhibit viability and promote apoptosis in LUAD via the miR‐181a‐5p/ETS1/STK16 axis