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. 2024 Jan 1;21(2):319–331. doi: 10.7150/ijms.89308

Figure 5.

Figure 5

The DLEU2/miR-212-5p/ELF3 axis in the anti-tumor effects of Huaier. (A) ELF3 3'UTR wild-type (wt) sequence containing the putative miR-212-5p binding sites and ELF3 3'UTR sequence with the mutant (mut) miR-212-5p binding sites. (B) ELF3 expression in lung adenocarcinoma compared to the noncancerous lung tissues from GEPIA database. (C) ELF3 expression in lung adenocarcinoma from UALCAN cancer database. (D and E) Luciferase reporter assay in HEK-293T. HEK-293T was cotransfected with pRL-TK carrying wild-type or mutant ELF3 3'UTR sequence and the miR-212-5p mimic or miR-212-5p inhibitor, and the luciferase activity was detected 48 h after transfection. (F) The western blot assay for ELF3 in A549 transfected with miR-212-5p mimic or miR-212-5p inhibitor. (G) The western blot assay for ELF3 in A549 cells transfected with pcDNA3.1-ELF3 (ELF3), DLEU2 siRNA (siDLEU2) or Huaier and the respective control. (H) Colony formation assay in DLEU2-silenced A549 cells transfected with pcDNA3.1-ELF3 (siDLEU2 + ELF3) or vector control (siDLEU2 + control). Colony formation assay in Huaier-treated A549 transfected with pcDNA3.1-ELF3 (Huaier + ELF3) or vector control (Huaier + control). (I and J) A549 cells were treated as in (H). wound healing assay (I), transwell assay (J) were performed. (K) The western blot assay for ELF3, Notch3, E-cadherin, Vimentin, MMP9 and VEGF in A549 cells treated as in (H).