Use of a glycolipid inhibitor to ameliorate renal cancer in a mouse model

PLoS One. 2013 May 9;8(5):e63726. doi: 10.1371/journal.pone.0063726. Print 2013.

Abstract

In a xenograft model wherein, live renal cancer cells were implanted under the kidney capsule in mice, revealed a 30-fold increase in tumor volume over a period of 26 days and this was accompanied with a 32-fold increase in the level of lactosylceramide (LacCer). Mice fed D- threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of glucosylceramide synthase and lactosylceramide synthase (LCS: β-1,4-GalT-V), showed marked reduction in tumor volume. This was accompanied by a decrease in the mass of lactosylceramide and an increase in glucosylceramide (GlcCer) level. Mechanistic studies revealed that D-PDMP inhibited cell proliferation and angiogenesis by inhibiting p44MAPK, p-AKT-1 pathway and mammalian target for rapamycin (mTOR). By linking glycosphingolipid synthesis with tumor growth, renal cancer progression and regression can be evaluated. Thus inhibiting glycosphingolipid synthesis can be a bonafide target to prevent the progression of other types of cancer.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Oral
  • Animals
  • Antigens, CD / metabolism
  • Blotting, Western
  • Disease Models, Animal*
  • Disease Progression
  • Enzyme Inhibitors / administration & dosage
  • Enzyme Inhibitors / pharmacology*
  • Galactosyltransferases / antagonists & inhibitors
  • Galactosyltransferases / metabolism
  • Glucosylceramides / metabolism
  • Glucosyltransferases / antagonists & inhibitors
  • Glucosyltransferases / metabolism
  • Kidney / drug effects*
  • Kidney / metabolism
  • Kidney / pathology
  • Kidney Neoplasms / drug therapy*
  • Kidney Neoplasms / metabolism
  • Kidney Neoplasms / pathology
  • Lactosylceramides / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Morpholines / administration & dosage
  • Morpholines / pharmacology*
  • Peptide Fragments / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / drug effects
  • Time Factors
  • Transcription Factors
  • Treatment Outcome
  • Tumor Burden / drug effects
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Antigens, CD
  • Enzyme Inhibitors
  • Glucosylceramides
  • Lactosylceramides
  • Morpholines
  • Peptide Fragments
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • WDR77 protein, mouse
  • CDw17 antigen
  • RV 538
  • Galactosyltransferases
  • Glucosyltransferases
  • UDPgalactose-glucosylceramide galactosyltransferase
  • ceramide glucosyltransferase
  • Proto-Oncogene Proteins c-akt