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Arylsulfatase B was recently studied as a potential biomarker of prostate cancer [1]

Halley's comet caused a famine [2]

Possible role in development of diabetes[edit]

Recent study showed that mice that consumed carrageenan in their drinking water had insulin resistance and abnormal glucose tolerance test. In addition, inhibition of the insulin receptor signaling pathway was demonstrated in the livers of carrageenan-fed mice and carrageenan-treated HepG2 cells. Results of the study demonstrate extra-colonic manifestations of carrageenan and suggest that carrageenan in the diet may contribute to development of diabetes [3]

Role in cystic fibrosis[edit]

Expression and activity of ARSB were found to be related to the function of cystic fibrosis transmembrane conductance regulator (CFTR), the membrane channel deficient in cystic fibrosis. Measurements in cystic fibrosis cell line IB3 and its derivative cell line C38, which has a functional CFTR, showed increased ARSB activity and expression in the C38 line. [4] CFTR potentiator VRT-532 increased ARSB expression and activity in cystic fibrosis cells to the level in the normal bronchial epithelial cells. [5]

Extra-lysosomal localization[edit]

Although primarily a lysosomal enzyme, ARSB was also found to localize at the cell membrane of hepatocytes, sinusoidal endothelial cells, and Kupffer cells in the liver, as well as in the apical membranes of normal and malignant colonic and prostatic epithelial cells, by immunohistochemistry and immunofluorescence studies. Membrane immunostaining in the colon and prostate was lower in malignant than in normal tissue and also was lower in higher grade malignancies. [6] [7] [8]

Role in malignancy[edit]

ARSB has been studied in a variety of cancers. Cultured normal mammary epithelial and myoepithelial cells had significantly higher ARSB activity than cultured malignant mammary cells. [9] Immunohistochemistry in the colon showed decreased membrane ARSB staining in colon cancer compared to normal colon, as well as in higher grade malignancies.[7] ARSB activity was lower in malignant than normal prostate tissue, and immunostaining of prostate tissue microarrays showed not only decreasing ARSB staining in prostate cancer tissue of a higher Gleason score, but also lower staining in patients with recurrent compared to non-recurrent cancer. ARSB staining was a greater predictor of recurrence than Prostate-specific antigen (PSA) test, indicating possible future role of ARSB as a prognostic biomarker of prostate cancer. [8] Further evidence of ARSB as a tumor suppressor was determined by molecular studies in cell cultures where ARSB was silenced by siRNA. The studies showed that decrease of ARSB leads to increase in free galectin-3, which attaches more strongly to less sulfated chondroitin 4-sulfate. Galectin-3 then acts on transcription factors AP-1 to increase expression of chondroitin sulfate proteoglycan versican and SP-1 to increase expression of WNT9A. [10] [11] Another mechanism by which reduced ARSB is associated with carcinogenesis is through increased binding of SHP2 to more sulfated chondroitin 4-sulfate, which leads to increased phosphorylation of p38 and MITF with subsequently increased expression of GPNMB.[12] In melanoma cells and normal melanocytes, ARSB silencing increased invasiveness and expression of CSPG4 and MMP2, known markers of melanoma progression. CSPG4 expression was mediated by reduced binding of galectin-3 to C4S, while MMP2 expression was mediated by increased binding of SHP2 to C4S. [13]

Role in metabolism[edit]

Reduced sulfate availability due to impaired activity of ARSB has been linked to increased aerobic glycolysis, as shown by an increase in NADH and NADPH, reduced oxygen consumption, increased extracellular acidification and serum lactate, and a decline in mitochondrial membrane potential in ARSB-silenced cells and ARSB-null mouse tissues. [14]


References[edit]

  1. ^ L Feferman, S Bhattacharyya, R Deaton, P Gann, G Guzman, A Kajdacsy-Balla and JK Tobacman. Arylsulfatase B (N-acetylgalactosamine-4-sulfatase): potential role as a biomarker in prostate cancer. Prostate Cancer and Prostatic Disease advance online publication, 9 July 2013; doi:10.1038/pcan.2013.18
  2. ^ Mike Wall. Why Halley's Comet May Be Linked to Famine 1,500 Years Ago. Life Science. December 19, 2013
  3. ^ S Bhattacharyya, I O-Sullivan, S Katyal, T Unterman,and JK Tobacman. Exposure to the common food additive carrageenan leads to glucose intolerance, insulin resistance and inhibition of insulin signalling in HepG2 cells and C57BL/6J mice. Diabetologia (2012) 55:194–203
  4. ^ Sumit Bhattacharyya, Dwight Look, Joanne K. Tobacman. Increased arylsulfatase B activity in cystic fibrosis cells following correction of CFTR. Clinica Chimica Acta, Volume 380, Issues 1–2, 1 May 2007, Pages 122–12
  5. ^ Sumit Bhattacharyya,Leo Feferman, Joanne K. Tobacman. Effect of CFTR modifiers on arylsulfatase B activity in cystic fibrosis and normal human bronchial epithelial cells. Pulmonary Pharmacology & Therapeutics 36 (2016)22-30
  6. ^ Keiko Mitsunaga-Nakatsubo, Shinichiro Kusunoki, Hayato Kawakami, Koji Akasaka, Yoshihiro Akimoto. Cell-surface arylsulfatase A and B on sinusoidal endothelial cells, hepatocytes, and Kupffer cells in mammalian livers. Med Mol Morphol (2009) 42:63–69 DOI 10.1007/s00795-009-0447-x
  7. ^ a b Sanjiv V. Prabhu, Sumit Bhattacharyya, Grace Guzman-Hartman, Virgilia Macias, André Kajdacsy-Balla, Joanne K. Tobacman. Extra-Lysosomal Localization of Arylsulfatase B in Human Colonic Epithelium. J Histochem Cytochem March 2011 vol. 59 no. 3 328-335 doi: 10.1369/0022155410395511
  8. ^ a b L Feferman, S Bhattacharyya, R Deaton, P Gann, G Guzman, A Kajdacsy-Balla, and JK Tobacman. Arylsulfatase B (N-acetylgalactosamine-4-sulfatase): potential role as a biomarker in prostate cancer. Prostate Cancer and Prostatic Disease (2013), 1–8
  9. ^ Sumit Bhattacharyyaa, Joanne K. Tobacman. Steroid sulfatase, arylsulfatases A and B, galactose-6-sulfatase, and iduronate sulfatase in mammary cells and effects of sulfated and non-sulfated estrogens on sulfatase activity. The Journal of Steroid Biochemistry and Molecular Biology. Volume 103, Issue 1, January 2007, Pages 20–34
  10. ^ S Bhattacharyya, L Feferman and JK Tobacman. Arylsulfatase B regulates versican expression by galectin-3 and AP-1 mediated transcriptional effects. Oncogene (2013), 1–10
  11. ^ Sumit Bhattacharyya, Leo Feferman and Joanne K. Tobacman. Increased Expression of Colonic Wnt9a through Sp-1 mediated Transcriptional Effects Involving Arylsulfatase B, Chondroitin-4-Sulfate, and Galectin-3. J. Biol. Chem. published online April 28, 2014
  12. ^ Sumit Bhattacharyya, Leo Feferman, Joanne K. Tobacman. Inhibition of Phosphatase Activity Follows Decline in Sulfatase Activity and Leads to Transcriptional Effects through Sustained Phosphorylation of Transcription Factor MITF. PLOS ONE April 14, 2016
  13. ^ Sumit Bhattacharyya, Leo Feferman, Kaoru Terai, Arkadiusz Z. Dudek, Joanne K. Tobacman. Decline in arylsulfatase B leads to increased invasiveness of melanoma cells. Oncotarget. December 1, 2016.
  14. ^ Sumit Bhattacharyya, Leo Feferman, Joanne K. Tobacman. Restriction of Aerobic Metabolism by Acquired or Innate Arylsulfatase B Deficiency: A New Approach to the Warburg Effect. Scientific Reports. September 8, 2016
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