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Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model

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Ral activation promotes melanomagenesis.

P A Zipfel¹, D C Brady, D F Kashatus

¹Department of Surgery, Duke University Medical Center, Durham, NC, USA.

|June 22, 2010

Summary

Small guanosine triphosphatase (GTPase) Ral proteins are activated in melanoma, regardless of NRAS or BRAF mutation status. Inhibiting RalA and RalB with short hairpin RNA (shRNA) reduced melanoma cell growth, indicating Rals promote tumorigenesis.

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Area of Science:

Oncology
Molecular Biology
Genetics

Background:

NRAS mutations drive approximately one-third of human melanomas.
Ras proteins activate Raf, PI3K, and RalGEF-Ral pathways.
Melanoma can activate Raf and PI3K pathways via BRAF mutations and PTEN loss.

Purpose of the Study:

To investigate the role of the RalGEF-Ral pathway in melanoma tumorigenesis.
To determine if RalA and RalB are activated in melanoma cells with different genetic backgrounds.

Main Methods:

Analysis of RalA activation in human melanoma cell lines.
Short hairpin RNA (shRNA)-mediated knockdown of RalA and RalB.
Assessment of the impact of RalA and RalB knockdown on melanoma cell growth.

Main Results:

RalA was activated in melanoma cell lines with NRAS mutations, BRAF mutations, or wild-type NRAS/BRAF.
Knockdown of RalA significantly inhibited melanoma cell growth across genotypes.
Knockdown of RalB also showed some inhibitory effects on melanoma cell growth.

Conclusions:

The RalGEF-Ral pathway, specifically RalA, is activated in melanoma irrespective of NRAS or BRAF mutation status.
RalA and RalB play a role in promoting melanoma cell tumorigenic growth.
Rals represent a potential therapeutic target in melanoma treatment.