miR-24-3p/FGFR3 Signaling as a Novel Axis Is Involved in Epithelial-Mesenchymal Transition and Regulates Lung Adenocarcinoma Progression

Figure 6

miR-24-3p inhibited growth and metastasis of lung adenocarcinoma cells and regulated EMT markers via FGFR3. (a) and (b) H1299 cells with stable overexpression of FGFR3 were transfected with miR-24-3p or miR-NC mimics, and their migration potentials were demonstrated by wound healing assays (). ns: not significant. (c) and (d) H1299 cells with stable overexpression of FGFR3 were transfected with miR-24-3p or miR-NC, and their migration and invasion potentials were demonstrated by the transwell assays (). (e) and (f) H1299 cells with stable FGFR3 overexpression were transfected with miR-24-3p or miR-NC mimics, and their proliferative ability was measured using colony formation assays. (g) H1299 cells transfected with miR-24-3p exhibited downregulated Snail and Vimentin expression and upregulated E-cadherin expression. H1299 cells with stable FGFR3 overexpression and transfection with miR-24-3p showed no significant alterations in Snail, Vimentin, and E-cadherin expression. (h) Western blot analysis of E-cadherin expression in lung adenocarcinoma tissues related to Figure 1(a). (i) Correlation analysis comparing FGFR3 and E-cadherin expression in 22 pairs of N and T samples corresponding to the cohort related to Figure 1(a). and .

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