Fig 1: DSE is specifically low expressed in melanoma patients.A Proteomics was used to analyze human melanoma and paracancerous tissues, and heat maps showed proteins specifically expressed in human melanoma tissues; B Volcanic maps showed differentially up-expressed (291) and down-expressed (301) proteins; C Combined analysis of specific expression in human melanoma and differential genes in human melanoma in TCGA; D qRT PCR analysis of mRNA levels of DSE in human melanoma and normal tissues (mean ± s.e.m. ***P < 0.001); E Western blot analysis of DSE levels in human melanoma and normal tissues; F The expression of DSE in human melanoma and normal tissues was analyzed by fluorescence staining (mean ± s.e.m. ***P < 0.001); G Expression of DSE protein in human melanoma cell line; H TCGA data were used to analyze the effect of DSE expression level on the prognosis of patients with human melanoma. Statistical significance was assessed by two-tailed unpaired Student’s t-test (D–G). Data are representative of three (D–G) independent experiments.
Fig 2: DSE inhibits melanoma growth and metastasis in vivo.A Analysis of the effect of DSE on tumor growth using cells overexpressing or knocking out DSE injected subcutaneously into nude mice (n = 4 mice, mean ± s.e.m. **P < 0.01); B Weight of tumor tissue in A (n = 4 mice, mean ± s.e.m. *P < 0.05, **P < 0.01); C, D Expression levels of Ki67 in tumor tissue in A (n = 4 mice, mean ± s.e.m. ***P < 0.001); E Tail vein injection of cells overexpressing or knocking out DSE into nude mice to analyze lung metastasis (n = 4 mice, mean ± s.e.m. **P < 0.01).
Fig 3: DSE regulates the expression of VCAN.A Transcriptome analysis of DSE-knockdown A875 cells; B Volcano plot showing differentially expressed genes in DSE-knockdown A875 cells; C–E VCAN protein and mRNA expression in DSE-overexpressing or knockdown cells level (mean ± s.e.m. **P < 0.01); F The correlation between DSE and VCAN expression in melanoma tissues was analyzed by immunofluorescence. Data are representative of three (C–E) independent experiments.
Fig 4: DSE regulates melanoma proliferation, invasion and migration through VCAN.A CCK8 assay to analyze the cell viability of A2508 cells overexpressing DSE and knocking out VCAN (mean ± s.e.m. **P < 0.01); B A2508 cells overexpressing DSE and knocking out VCAN were injected into nude mice to observe tumor growth; (n = 4 mice, mean ± s.e.m. **P < 0.01 and ***P < 0.001); C tumor weight in B (n = 4 mice, mean ± s.e.m. **P < 0.01); D Transwell assay analyzing DSE overexpressing and VCAN knockout Invasion and migration of A2508 cells (mean ± s.e.m. **P < 0.01); E Tail vein injection of cells overexpressing or knocking out DSE into nude mice to analyze lung metastasis (n = 4 mice, mean ± s.e.m. **P < 0.01 and ***P < 0.001). Data are representative of three (A–D) independent experiments.
Fig 5: DSE inhibits proliferation, invasion and migration of melanoma cells.A A2508 cells were infected with lentivirus (PLVE) and DSE, respectively, and the expression levels of DSE protein in cells were analyzed by western blotting; B CCK8 assay to analysis cell viability of A2508 cells stably overexpressing DSE (mean ± s.e.m. *P < 0.05); C Colony formation assay to analyze cell proliferation of A2508 cells stably overexpressing DSE; (mean ± s.e.m. ***P < 0.001); D Transwell assay to analyze cell invasion and migration of A25O8 cells stably overexpressing DSE (mean ± s.e.m. **P < 0.01); E Knockdown of DSE in A875 cells and Western blot analysis of DSE protein expression levels in those cells; F CCK8 assay was used to analyze the cell viability of DSE knockout A875 cells; (mean ± s.e.m. **P < 0.01); G Colony formation assay to analyze cell proliferation of DSE knockout A875 cells (mean ± s.e.m. ***P < 0.001); H Transwell assay to analyze cell invasion and migration of DSE knockout A875 cells (mean ± s.e.m. **P < 0.01). Data are representative of three (A–H) independent experiments.
Supplier Page from MilliporeSigma for Anti-DSE antibody produced in rabbit