Fig 1: Survival analysis of four candidate hub genes in TCGA-BLCA and GSE19915 data. (A–D) Survival analysis result of CORO1C (A), TMPRSS4 (B), PIK3C2B (C), and ZNF692 (D) in TCGA-BLCA downloaded from GEPIA. (E–G) Survival analysis of CORO1C (E), TMPRSS4 (F), and ZNF692 (G) in GSE19915.
Fig 2: Immunohistochemical staining for TMPRSS4 in human non-small cell lung cancer at ×20 magnification. High expression of TMPRSS4 in LUSC cells (black arrowhead) with a lesser expression in (A) the adjacent peritumoral tissue, and a high expression in alveolar epithelial cells (red arrowhead) in (B) the NAT of a male patient (53 years of age, T2N0M0; grade 2, stage IB). (C) Lesser, but detectable staining of TMPRSS4 in lung squamous cell carcinoma cells (black arrowhead) with minor staining in the adjacent peritumoral tissue, and (D) a high expression on alveolar epithelial cells (red arrowhead) in the NAT of a female patient (56 years of age, T2N0M0; grade 3, stage IIIA). Protein expression in lung adenocarcinoma cells (black arrowhead) with (E) a lesser expression in the adjacent peritumoral tissue (LUAD) and (F) a high expression on alveolar epithelial cells (red arrowhead) in cancer adjacent lung tissue (AT) of a male patient (65 years of age, T2N2M0, grade 3, stage IIIA). (G) Expression in LUAD (black arrowhead) and a (H) high expression on both bronchial (blue arrowhead) and alveolar epithelial cells (red arrowhead) in cancer adjacent lung tissue of a female patient (35 years of age, T4N1M0, grade 3, stage IIIA). Scale bar, 500 nm. TMPRSS4, transmembrane protease serine 4; LUSC, lung squamous cell carcinoma; LUAD, lung adenocarcinoma; NAT, normal adjacent tissue; AT, adjacent tissue.
Fig 3: Validation of the prognostic value of four candidate hub genes in clinical specimens. (A–D) Survival analysis of CORO1C (A), TMPRSS4 (B), PIK3C2B (C), and ZNF692 (D) in 124 bladder cancer patients' follow-up in our center. (E–L) Representative image of 200× immunohistochemical experiment on CORO1C (E,F), TMPRSS4 (G,H), PIK3C2B (I,J), and ZNF692 (K,L) clinical specimens.
Fig 4: Silencing of TMPRSS4 or overexpression of miR-125a-5p inhibits the NF-?B signaling pathway in NCI-H358 cells. The phosphorylation of I?B was decreased with an increase in I?B expression in the si-TMPRSS4 group and mimics group, and cytoplasmic NF-?B expression was increased along with a decrease in nuclear NF-?B expression. These data indicated that the silencing of TMPRSS4 or the upregulation of miR-125a-5p may inhibit the activation of the NF-?B signaling pathway. Moreover, the expression of Bcl-2, which is the direct transduction effector of NF-?B signaling pathway, was also inhibited by si-TMPRSS4 or the overexpression of miR-125a-5p.
Fig 5: Hallmark GSEA and EMT GSVA of hub genes based on TCGA-BLCA mRNA data. Some representative top enriched pathways of CORO1C were (A) epithelial to mesenchymal transition pathway, (B) angiogenesis pathway, and (C) hypoxia pathway. Only one downregulated GSEA result of TMPRSS4 enriched in (D) mesenchymal transition pathway. (E) GSVA pathway score of mesenchymal state gene set and (F) epithelial state gene set vs. normalized Log2(FPKM + 1) expression of CORO1C. (G) GSVA pathway score of mesenchymal state gene set and (H) epithelial state gene set vs. normalized Log2(FPKM + 1) expression of TMPRSS4.
Supplier Page from Abcam for Anti-TMPRSS4 antibody