Fig. 5: TFAP2A promotes LUAD metastasis by transactivating PSG9 to potentiate TGF-β signaling. | Cell Death & Disease

Fig. 5: TFAP2A promotes LUAD metastasis by transactivating PSG9 to potentiate TGF-β signaling.

From: TFAP2A potentiates lung adenocarcinoma metastasis by a novel miR-16 family/TFAP2A/PSG9/TGF-β signaling pathway

Fig. 5

A 515 Patients in TCGA-LUAD dataset were divided equably into high, middle and low group based on TFAP2A expression. B Volcano plot exhibiting differentially expressed genes (DEGs) between TFAP2A high and low expression groups. C p-values and coefficients(r) of expression correlation analysis between TFAP2A and DEGs described in B, DEGs with p < 0.05 and r>0.3 or r < -0.3 were regarded significant, further DEGs with TFAP2A-ChIP-Seq evidence in hTFtarget database were picked out and texted. D Transcripts levels of seven identified possibly TFAP2A-targeted genes in TFAP2A overexpression cell models of PC-9. E PSG9 transcript levels in TFAP2A knockdown cell models of PC-9. F, G PSG9 transcript levels in TFAP2A overexpression and knockdown cell models of H1650 (F, overexpression vs. control; G, knockdown vs. control). H TFAP2A and PSG9 protein levels for TFAP2A knockdown and overexpression cell models of PC-9 (left) and H1650 (right). I TFAP2A protein expression for TFAP2A overexpression cell models of HEK293T. J Effects for TFAP2A overexpression upon luciferase activity in HEK293T transfected with pGL3-Basic and pGL3-PSG9-promoter luciferase reporter (pc-TFAP2A vs. pc-NC). K Relative levels of immunoprecipitated PSG9 promoter regions (compared to Input chromatin) among positive control (Anti-Histone 3), negative control (Anti-IgG) and experiment group (Anti-TFAP2A) detected by qPCR. L EMT markers (E-cadherin/N-cadherin protein expression) and TGF-β signaling status (Phospho-Smad2S465/467/Smad2 protein expression) between PSG9 knockdown (si-PSG9) and control (si-NC) H1650 with stable TFAP2A overexpression. M Migratory and invasive abilities between PSG9 knockdown (si-PSG9) and control (si-NC) H1650 with stable TFAP2A over-expression. N EMT markers (E-cadherin/ N-cadherin protein expression) and TGF-β signaling status (Phospho-Smad2S465/467/Smad2 protein expression) between PSG9 overexpression (pc-PSG9) and control (pc-NC) PC-9 with stable TFAP2A knockdown. O Migratory and invasive abilities between PSG9 overexpression (pc-PSG9) and control (pc-NC) PC-9 with stable TFAP2A knockdown. P EMT markers (E-cadherin/ N-cadherin protein expression) and TGF-β signaling status (Phospho-Smad2S465/467/Smad2 protein expression) among control (pc-NC + DMSO), PSG9 overexpression (pc-PSG9 + DMSO), and PSG9 overexpression treated with TGF-β inhibitor (pc-PSG9 + SB431542) PC-9 with stable TFAP2A knockdown. *p < 0.05; **p < 0.01; ***p < 0.001. N≥3, Data are presented as mean ± SD or through boxplots.

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