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Fig. 4 | Journal of Hematology & Oncology

Fig. 4

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

Fig. 4

AS-tDR-007333 enhances NSCLC cell proliferation through up-regulating MED29. A RNA-seq revealed the differentially regulated genes between AS-tDR-007333-overexpression cells and control cells. B Principal component analysis (PCA) showed a clear difference between genetic components of AS-tDR-007333-overexpression cells and that of control cells. C Top ten differentially expressed genes regulated by AS-tDR-007333, with MED29 displaying the highest fold change and smallest P value. D Gene Ontology (GO) analysis revealed that AS-tDR-007333 was significantly correlated with mediator complex (MED) pathway genes. E MED29 gene was significantly up-regulated in NSCLC tumor tissues compared with that in adjacent tissues (analysis on TCGA data). F The expression levels of MED29 gene and protein in NSCLC cells were significantly higher than that in BEAS-2B cells. G Western blot analysis showed that overexpression of AS-tDR-007333 promoted MED29 protein expression in both PC9 and A549 cells, while knockdown of AS-tDR-007333 suppressed MED29 protein expression. Numerical numbers denoted the ratio of integrated optical density (IOD) of MED29/IOD of β-actin. H, I Up-regulation of MED29 promoted cell proliferation of NSCLC cells. J, K Knockdown of MED29 expression inhibited NSCLC cell proliferation. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001

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