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. 2023 Aug 2;11(3):101065. doi: 10.1016/j.gendis.2023.06.034

Figure 2.

Figure 2

LKB1 depletion in ATII cells induces EMT. (A) The Gene Set Enrichment Analysis (GSEA) plot showing the enrichment of Hallmark_Epithelial–Mesenchymal Transition in LKB1-depleted ATII cells. Normalized enrichment score (NES) and false discovery rate (FDR) are indicated. (B) The RNA-seq data showing relative expressions of CDH1 (encoding E-cadherin), VIM (encoding Vimentin), SNAI1 (encoding Snail1), SNAI2 (encoding Snail2), TWIST1, ZEB1, and ZEB2 in LKB1-depleted ATII cells versus control. The data were expressed as mean ± standard deviation. n = 3 samples in each group; ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001; ns, not significant. (C) Relative fold changes in mRNA levels of CDH1 (E-cadherin), VIM (Vimentin), SNAI1 (Snail1), SNAI2 (Snail2), TWIST1, ZEB1, and ZEB2 in LKB1-depleted ATII cells versus control. ACTB (encoding β-actin)-normalized mRNA levels in ATII cells were used to set the baseline value at unity. The data were expressed as mean ± standard deviation. n = 3 samples in each group; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001; ns, not significant. (D) Protein expressions of E-cadherin, Snail2, and LKB1 in ATII cells transfected with the indicated siRNA. β-Tubulin was used as a loading control.