Fig 1: ADAMTS12 expression is significantly upregulated in BCa.A, DEGs in the TCGA-BLCA dataset were determined employing a Volcano plot. B and C, ADAMTS12 mRNA expression levels in BCa and healthy tissues were examined employing data from TCGA-BLCA. D and E, ADAMTS12 expression in various malignancy types was examined utilizing data from the TCGA. F, the levels of ADAMTS12 in BCa samples and nearby healthy tissues were analyzed employing western blotting (n = 3). G, the levels of ADAMTS12 in BCa samples and nearby healthy tissues were analyzed employing qRT-PCR (n = 31). The data are presented as the mean ± SD. Unpaired t tests were employed to compare two groups. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ns, no statistical difference.
Fig 2: ADAMTS12 promotes tumor growth and triggers FAK/PI3K/AKT signaling pathway activation in BCa in vivo.A, the T24 cells transfected with shNC or shADAMTS12 were used to generate subcutaneous xenograft tumors. B, the xenograft tumor volumes in the shNC group and shADAMTS12 group were measured (n = 3 respectively). C, the weights of xenograft tumors in the shNC group and shADAMTS12 group were measured (n = 3 respectively). D, the expression levels of COL3A1, p-FAK, FAK, p-PI3K, PI3K, p-AKT, and AKT were determined in the BCa xenograft tissues by Western blotting analysis (n = 3 respectively). The data are presented as the mean ± SD. Unpaired t-tests were employed to compare two groups. ∗p < 0.05.
Fig 3: ADAMTS12 promotes migration and invasion in BCa cells.A and B, Wound-healing assay demonstrated that the upregulation of ADAMTS12 expression in T24 cells promoted cell migration, whereas the downregulation of ADAMTS12 expression in T24 cells inhibited cell migration (n = 3 respectively). C and D, transwell assay demonstrated that ADAMTS12 overexpression in T24 cells significantly enhanced invasion, whereas ADAMTS12 expression knockdown in T24 cells effectively suppressed invasion (n = 3 respectively). The data are presented as the mean ± SD. Unpaired t tests were employed to compare two groups. ∗p < 0.05.
Fig 4: ADAMTS12 facilitates the growth and suppresses the apoptosis of BCa cells.A and B, ADAMTS12 levels were assessed in BCa cell lines (T24, UMUC3, 5637) and a non-cancerous cell line (SV-HUC-1) utilizing qRT-PCR and western blotting techniques (n = 3 respectively). C–F, the effects of ADAMTS12 overexpression and knockdown in T24 cells were evaluated using Western blotting and qRT-PCR analysis for validation purposes. G and H, T24 cell viability was examined employing the CCK-8 assay after knockdown and overexpression of ADAMTS12, respectively (n = 3 respectively). I and J, the apoptotic rate of cells was assessed by flow cytometry following knockdown and overexpression of ADAMTS12, respectively (n = 3 respectively). The data are presented as the mean ± SD. Unpaired t-tests were employed to compare the two groups. One-way ANOVAs with the Tukey test were used for comparisons involving more than two groups. ∗p < 0.05; ∗∗p < 0.01.
Fig 5: ADAMTS12-associated genes identification using the TCGA-BLCA dataset and functional enrichment analysis.A, the TCGA-BLCA dataset was utilized to identify genes associated with ADAMTS12 using the volcano plot. B and C, the genes that exhibited a positive correlation with ADAMTS12 in BCa were subjected to comprehensive KEGG and GO analyses. D and E, the genes that showed a negative correlation with ADAMTS12 in BCa were analyzed using KEGG and GO analyses. GO analysis included biological process (BP), cellular component (CC), and molecular function (MF).
Supplier Page from Abcam for Anti-ADAMTS12 antibody