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Fig. 9 | Diagnostic Pathology

Fig. 9

From: Diagnostic potential of NRG1 in benign nerve sheath tumors and its influence on the PI3K-Akt signaling and tumor immunity

Fig. 9

Validation of NRG1-mediated cell behavior through the PI3K/AKT signaling pathway using cell line models. A RT-qPCR detection of NRG1 knockdown efficiency. B Western blot detection of NRG1 knockdown efficiency and expression levels of critical proteins in the PI3K/AKT signaling pathway. Statistical graphs on the right. C Western blot detection of critical proteins in the PI3K/AKT signaling pathway in cells treated with a PI3K inhibitor. Statistical graphs on the right. D Cell cycle of cells after NRG1 knockdown and PI3K inhibitor treatment detected by flow cytometry. Statistical graphs on the right. E After NRG1 knockdown and PI3K inhibitor treatment, apoptosis proportions of cells were detected by flow cytometry. Statistical graph in the first quadrant. F Cell migration ability after NRG1 knockdown and PI3K inhibitor treatment detected by Transwell assay. G Expression levels of critical proteins in the PI3K/AKT signaling pathway in cells treated with a PI3K agonist after NRG1 knockdown detected by Western blot. Statistical graphs on the right. H Cell cycle changes of cells after NRG1 knockdown and PI3K agonist treatment detected by flow cytometry. Statistical graphs on the right. I After NRG1 knockdown and PI3K agonist treatment, apoptosis of cells was detected by flow cytometry. Statistical graph in the first quadrant. J Cell migration ability after NRG1 knockdown and PI3K agonist treatment detected by Transwell assay. Indicates a difference compared to sh-NC or con or sh-Nrg1 + DMSO, where P  < 0.05, indicates a difference compared to sh-NC or DMSO or sh-Nrg1 + DMSO, P  < 0.01, and indicates a difference compared to sh-NC or DMSO or sh-Nrg1 + DMSO, P  < 0.001, ** indicates a difference compared to sh-NC or DMSO or sh-Nrg1 + DMSO, P  < 0.0001

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