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. 2020 Jun 16;11(24):2327–2344. doi: 10.18632/oncotarget.27634

Figure 7. Overall connected pathways of chondroitin 4-sulfate (C4S), chondroitin-4,6-disulfate (CSE), ARSB, and GALNS which may contribute to EMT and progressive increase in SHP2 inhibition.

Figure 7

In malignant prostate epithelium, ARSB increased and GALNS declined, in association with increase in CHST15. This pathway may contribute to continuing increases in CHST15 and chondroitin 4-sulfate (C4S), due to inhibition of SHP2 and activation of Wnt signaling through a non-canonical pathway. Noting higher C4S in stroma, with higher C6S in normal epithelium, a relative increase in C4S suggests potential for epithelial to mesenchymal transition in the epithelium. In the normal epithelium, CHST11 expression is less than in stroma and CHST3, leading to C6S, is higher. These findings are consistent with the disaccharide analysis showing lower 4S and higher 6S disaccharides in the prostate epithelial cells. [ARSB = arylsulfatase B; C4S = chondroitin 4-sulfate; C6S = chondroitin 6 = sulfate; CHST = chondroitin sulfotransferase; DKK = Dickkopf Wnt signaling pathway inhibitor; ERK = extracellular regulated kinase; GALNS = N-acetylgalactosamine-6-sulfatase; SHP2 = PTPN11 = non-receptor tyrosine phosphatase 2].