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10.18632/oncotarget.12996

http://scihub22266oqcxt.onion/10.18632/oncotarget.12996
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C5356675!5356675 !27806323
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suck abstract from ncbi


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pmid27806323
      Oncotarget 2016 ; 7 (51 ): 84486-84495
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  • Human sulfatase 1 exerts anti-tumor activity by inhibiting the AKT/ CDK4 signaling pathway in melanoma #MMPMID27806323
  • Lou X ; Sun B ; Song J ; Wang Y ; Jiang J ; Xu Y ; Ren Z ; Su C
  • Oncotarget 2016[Dec]; 7 (51 ): 84486-84495 PMID27806323 show ga
  • Human sulfatase 1 (hSulf-1) has aryl sulfatase activity. It can reduce the sulfation of cell surface heparan sulfate proteoglycan (HSPG) and inhibit various growth factor receptor-mediated signaling pathways. In most cancers, hSulf-1 is inactivated, which endows cancer cells with increasesed cell proliferation and metastatic activities, inhibition of apoptosis, and decreased sensitivity to radio- and chemotherapy. In this study, we found that hSulf-1 overexpression in melanoma cells can inhibit cell proliferation and induce cell cycle arrest and apoptosis by decreasing the protein kinase B (AKT) phosphorylation and limiting CDK4 nuclear import. We further confirmed that hSulf-1 overexpression can inhibit AKT phosphorylation and CDK4 nuclear localization and retard the growth of melanoma xenograft tumors in nude mice. Overall, hSulf-1 function in melanoma cells provides an ideal molecular treatment target. An important anti-tumor mechanism of hSulf-1 operates by decreasing downstream AKT signaling pathway activity and inhibiting the nuclear import of CDK4.
  • |Active Transport, Cell Nucleus [MESH]
  • |Animals [MESH]
  • |Apoptosis/genetics [MESH]
  • |Cell Cycle Checkpoints/genetics [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Proliferation/genetics [MESH]
  • |Cyclin-Dependent Kinase 4/*genetics/metabolism [MESH]
  • |Gene Expression Regulation, Neoplastic [MESH]
  • |Humans [MESH]
  • |Male [MESH]
  • |Melanoma/*genetics/metabolism/pathology [MESH]
  • |Mice, Inbred BALB C [MESH]
  • |Mice, Nude [MESH]
  • |Phosphorylation [MESH]
  • |Proto-Oncogene Proteins c-akt/*genetics/metabolism [MESH]
  • |RNA Interference [MESH]
  • |Signal Transduction/*genetics [MESH]
  • |Sulfotransferases/*genetics/metabolism [MESH]


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