Fig 2: Variation of TNXB mRNA expression in tumors versus normal or adjacent tissues.Cancers of high incidence/mortality were studied (A and C), as well as cancers for which TNX status had been previously studied (B and D). A and B: Expression values of TNXB mRNA obtained from the selected datasets extracted from the GEO database. Non-parametric paired (breast, stomach, liver, and kidney cancers) and unpaired (lung, prostate, colon, glioma, ovary, melanoma and leiomyoma cancers) tests were performed comparing tumoral to normal tissues. For datasets comparing TNXB mRNA expression in tumoral sample versus adjacent normal tissue, a bar chart is presented just below the first graphical representation. Each bar corresponds to a patient and is either blue, when TNXB mRNA expression is downregulated in tumoral sample or red, when TNXB expression is upregulated. C and D: Expression data and associated p-values extracted from the UALCAN web-portal. Numbers of tumoral and control samples for each dataset are indicated. ****p < 0.0001; ***p < 0.001; **p < 0.01 and *p < 0.05.

Fig 3: High-confidence interaction among extracellular matrix (ECM)–related proteins and greater fibrosis in adult dilated cardiomyopathy (DCM) hearts compared with pediatric DCM hearts. A, STRING (Search Tool for the Retrieval of Interacting Genes/Proteins) analysis shows high-confidence interaction clusters (k-means=5 clusters indicated by node color) formed by ECM-related proteins. B through D, Representative images of Picrosirius Red (PSR) (B) and Masson trichrome–stained (C) left ventricular free wall from pediatric and adult control and DCM myocardium. Scale bar: 100 µm. D, Averaged quantification of collagen content (from PSR-stained sections) in indicated groups (mean±SEM). n=6 hearts per group. *P<0.05 compared with the corresponding control, † P<0.05 compared with the corresponding pediatric group. ADAM indicates a disintegrin and metalloprotease; ADAMTS, a disintegrin and metalloproteinase with thrombospondin motifs; AFU, arbitrary fluorescence units; BGN, biglycan; COL, collagen; DCN, decorin; LUM, lumican; MMP, matrix metalloprotease; NFC, nonfailing control; OGN, osteoglycan; SGCG, sarcoglycan gamma; SPARC, secreted protein acidic and cysteine-rich; THBS1, thrombosondin-1; TIMP, tissue inhibitors of metalloprotease; TNXB, tenascin x; VCAN, versican.

Fig 4: Prognosis according to TNXB expression level in tumors.TNXB mRNA levels at various stages or grades of tumor progression in lung adenocarcinoma (A), breast cancer (B) and glioma (C). Comparison of survival probability of patients with TNXBlowversus TNXBhigh mRNA expression in lung (D) and breast (E) tumors by Kaplan–Meier method. Groups were delimitated by median cut-off according to TNXB expression values in tumoral samples.

Fig 5: Expressions of TNXB was up-regulated due to LncRNA LINC01305 silencing. Expressions of genes in SiHa, Hela and C-33A were expressed as mean ± SD (n = 3), and compared using one-way ANOVA. *P < 0.05 compared with the blank group, RT-qPCR, reverse transcription quantitative polymerase chain reaction. TNXB, Tenascin-X B; NC, negative control