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A 3D Organotypic Melanoma Spheroid Skin Model
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Functional RET G691S polymorphism in cutaneous malignant melanoma.

N Narita1, A Tanemura, R Murali

  • 1Department of Molecular Oncology, John Wayne Cancer Institute at Saint John's Health Center, Santa Monica, CA 90404, USA.

Oncogene
|June 30, 2009
PubMed
Summary

The RET proto-oncogene polymorphism (RETp) is more common in desmoplastic melanomas and drives tumor progression. Glial cell line-derived neurotrophic factor (GDNF) amplifies proliferation and invasion in RETp melanoma cells.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The RET proto-oncogene encodes a receptor tyrosine kinase activated by glial cell line-derived neurotrophic factor (GDNF).
  • A specific RET polymorphism (RETp) in the juxtamembrane region is a germline variant.
  • Cutaneous melanomas, especially desmoplastic melanomas (DMs), exhibit neurotropic properties.

Purpose of the Study:

  • To determine the frequency of RETp in cutaneous melanoma subtypes.
  • To investigate the functional response of RETp-harboring melanoma cells to GDNF stimulation.

Main Methods:

  • Assessed RETp frequency in 71 non-desmoplastic melanomas (non-DMs) and 70 DMs.
  • Utilized melanoma cell lines with RETp, wild-type RET (RETwt), BRAF V600E mutation (BRAFmt), or wild-type BRAF (BRAFwt).
  • Evaluated cell proliferation, migration, invasion, and signaling pathway activation (ERK, Akt) upon GDNF stimulation.

Main Results:

  • RETp frequency was significantly higher in DMs (61%) compared to non-DMs (31%, P<0.001).
  • BRAFmt was infrequent in DMs (11%).
  • GDNF significantly enhanced proliferation, migration, and invasion in RETp cells, but not RETwt cells, activating ERK and Akt pathways.

Conclusions:

  • RETp is a frequent germline polymorphism in cutaneous melanoma, particularly in desmoplastic subtypes.
  • GDNF stimulation of RETp melanoma cells promotes tumor progression via enhanced proliferation, migration, and invasion.
  • The GDNF-RETp pathway's pro-tumorigenic effects are independent of BRAFmt status.