IMP4 Silencing Inhibits the Malignancy of Lung Adenocarcinoma via ERK Pathway

Figure 6

IMP4 overexpression promoted the malignant phenotypes via activating the ERK pathway in LUAD cells. ((a) and (b)) The potential pathways which IMP4 could regulate in LUAD were analysed using GSEA. (c) After transfection of A549 and H1299 cells with si-IMP4-1 and si-IMP4-2, the expression of MEK, p-MEK, ERK, and p-ERK was analysed using Western blotting. (d) The expression of MEK, p-MEK, ERK, and p-ERK in subcutaneous tumour tissues were analysed using Western blotting. (e) Immunohistochemistry was applied to assess p-ERK1/2 and p-MEK1 levels in subcutaneous tumour. (f) After transfection of A549 cells with pcDNA3.1-IMP4, qRT-PCR was applied to assess IMP4 levels. After transfection with pcDNA3.1-IMP4 or treatment with SCH772984, in A549 cell proliferation was evaluated using the CKK-8 (g) and EdU (h); (i) After transfection with pcDNA3.1-IMP4 or treatment with SCH772984, A549 cell cycle was assessed using flow cytometry. (j) After transfection with pcDNA3.1-IMP4 or treatment with SCH772984, A549 cell invasion was assessed using transwell. , ; , .

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