Expression of Hedgehog ligand and signal transduction components in mutually distinct isocitrate dehydrogenase mutant glioma cells supports a role for paracrine signaling
Copyright policy )Expression of Hedgehog ligand and signal transduction components in mutually distinct isocitrate dehydrogenase mutant glioma cells supports a role for paracrine signaling
Hedgehog (Hh) signaling regulates the growth of malignant gliomas by a ligand-dependent mechanism. The cellular source of Sonic Hh ligand and mode of signaling have not been clearly defined due to the lack of methods to definitively identify neoplastic cells in glioma specimens. Using an antibody specific for mutant isocitrate dehydrogenase protein expression to identify glioma cells, we demonstrate that Sonic Hh ligand and the pathway components Patched1 (PTCH1) and GLI1 are expressed in neoplastic cells. Further, Sonic Hh ligand and its transcriptional targets, PTCH1 and GLI1, are expressed in mutually distinct populations of neoplastic cells. These findings support a paracrine mode of intratumoral Hh signaling in malignant gliomas.
- Vanderbilt University United States
- Vanderbilt University Medical Center United States
- Vanderbilt-Ingram Cancer Center United States
Patched Receptors, Fluorescent Antibody Technique, Receptors, Cell Surface, Glioma, Zinc Finger Protein GLI1, Isocitrate Dehydrogenase, Patched-1 Receptor, Mutation, Paracrine Communication, Humans, Hedgehog Proteins, In Situ Hybridization, Signal Transduction, Transcription Factors
Patched Receptors, Fluorescent Antibody Technique, Receptors, Cell Surface, Glioma, Zinc Finger Protein GLI1, Isocitrate Dehydrogenase, Patched-1 Receptor, Mutation, Paracrine Communication, Humans, Hedgehog Proteins, In Situ Hybridization, Signal Transduction, Transcription Factors
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