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- Product number
- PA5-43331 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- SULF2 Polyclonal Antibody
- Antibody type
- Polyclonal
- Antigen
- Synthetic peptide
- Description
- Peptide sequence: DVLNQLHVQL MELRSCKGYK QCNPRTRNMD LGLKDGGSYE QYRQFQRRKW
- Concentration
- 1 mg/mL
Submitted references Sulfatase 2-Induced Cancer-Associated Fibroblasts Promote Hepatocellular Carcinoma Progression via Inhibition of Apoptosis and Induction of Epithelial-to-Mesenchymal Transition.
Wang C, Shang C, Gai X, Song T, Han S, Liu Q, Zheng X
Frontiers in cell and developmental biology 2021;9:631931
Frontiers in cell and developmental biology 2021;9:631931
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Supportive validation
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- Invitrogen Antibodies (provider)
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- Experimental details
- Western blot analysis of human HepG2 cell lysate using an anti-Sulfatase 2 polyclonal antibody (Product # PA5-43331).
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunohistochemistry analysis of human kidney tissue using an anti-Sulfatase 2 polyclonal antibody (Product # PA5-43331).
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
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- Experimental details
- FIGURE 1 SULF2 expression in HCC tissues was related positively with CAF markers, which predicted poor prognosis after surgery. (A) TCGA database showed that SULF2 mRNA in HCC tissues was significantly associated positively with alpha-SMA ( r = 0.512, P < 0.01), FAP ( r = 0.654, P < 0.01), and POSTN ( r = 0.512, P < 0.01). (B) The further analysis of TCGA database displayed that CAF markers, including alpha-SMA ( P < 0.0045), FAP ( P = 0.012), and POSTN ( P = 0.006), were significantly associated with the worse prognosis of HCC patients. (C) IHC staining assay about 102 HCC samples collected from our hospital showed that SULF2 expression was positively associated with alpha-SMA ( r = 0.731, P < 0.001), FAP ( r = 0.658, P < 0.001), and POSTN ( r = 0.848, P < 0.01), respectively. SULF2, sulfatase 2; HCC, hepatocellular carcinoma; CAF, carcinoma-associated fibroblast; TCGA, The Cancer Genome Atlas; IHC, immunohistochemical.
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- Invitrogen Antibodies (provider)
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- Experimental details
- FIGURE 4 CAFs activated SDF-1/CXCR4/PI3K/AKT pathway and consequently inhibited HCC cell apoptosis. (A) Both RT-PCR and western immunoblotting assays showed that LX2 SULF2 cells expressed significantly more SDF-1 than LX2 Vector cells. Cell fractions: LX2 cells. (B) It was found by ELISA assay that there was more SDF-1 protein in conditioned medium from LX2 SULF2 cells than that from LX2 Vector cells (the protein was extracted from total cells). (C) Microarray profiling of mRNA expression showed that most downstream genes of SDF-1/CXCR4 signaling were remarkably upregulated in Hep3B CAFs cells in contrast to Hep3B Vector cells. (D) Co-culture with CAFs was found by western immunoblotting to increase expression of SDF-1, CXCR4, p-PI3K, and p-AKT in Hep3B cells, while treatment of CXCR4 inhibitor (AMD3100) did not alter the expression of phosphorylation of PI3K, AKT, BAD, caspase 9, and FKHRL 1 in Hep3B cells. Cell fractions: Hep 3B cells (the protein was extracted from total cells). (E) By both DAPI staining and caspase 3/7 activity assay, it was found that co-culture with CAFs suppressed cell apoptosis, whereas AMD3100 treatment did not influence Hep3B cell apoptosis apparently. CAF, carcinoma-associated fibroblast; HCC, hepatocellular carcinoma; SULF2, sulfatase 2.
