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Fig. 7 | Journal of Hematology & Oncology

Fig. 7

From: A novel tRNA-derived fragment AS-tDR-007333 promotes the malignancy of NSCLC via the HSPB1/MED29 and ELK4/MED29 axes

Fig. 7

AS-tDR-00733 regulates MED29 through ELK4-mediated transcriptional activation. A Schematic view of the putative binding sites and sequences of ELK4 on MED29 promoter region, predicted by the JASPAR and UCSC websites. B Inhibitive effect of si-ELK4 on PC9 cell proliferation. C The impact of ELK4 knockdown by si-ELK4 on A549 cell proliferation. D AS-tDR-007333 increased ELK4 protein expression levels in A549 and PC9 cells (upper); AS-tDR-007333-inhibitor repressed the expression of ELK4 protein in NSCLC cells (lower). E Up-regulation of AS-tDR-007333 promoted the expression of ELK4 gene in NSCLC cells. F AS-tDR-007333-inhibitor suppressed ELK4 gene expression in NSCLC cells. G Interaction effects between si-ELK4 and AS-tDR-007333 on PC9 cell proliferation. H Co-transfection of si-ELK4 and AS-tDR-007333 inhibited the promoting effect of AS-tDR-007333 on A549 cell proliferation. I ChIP-PCR assay verified the reliability of the binding sequences of ELK4 on MED29 promoter region. J Luciferase reporter gene assays showed that binding of ELK4 to the wild-type MED29 promoter significantly increased the transcription of MED29. *P < 0.05; **P < 0.01; ***P < 0.001

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