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J Invest Dermatol. 2014 May;134(5):1359-1368. doi: 10.1038/jid.2013.511. Epub 2013 Nov 28.

A tumor suppressor function for the lipid phosphatase INPP4B in melanocytic neoplasms.

Author information

1
Department of Dermatology, Columbia University Medical Center, New York, New York, USA.
2
Department of Pathology and Cell Biology, Columbia University Medical Center, New York, New York, USA.
3
Institute for Cancer Genetics, Columbia University, New York, New York, USA.
4
Department of Dermatology, Fachklinik Hornheide at University Muenster, Muenster, Germany.
5
Department of Cancer Research, Fachklinik Hornheide at University Muenster, Muenster, Germany.
6
Department of Dermatology, Columbia University Medical Center, New York, New York, USA; Department of Pathology and Cell Biology, Columbia University Medical Center, New York, New York, USA. Electronic address: bh2179@cumc.columbia.edu.

Abstract

The phosphoinositide-3 kinase (PI3K) pathway is deregulated in a significant proportion of melanomas, and PI3K pathway activation in combination with constitutively active mitogen-activated protein kinase signaling shows synergistic effects in the process of melanoma tumorigenesis. Recently, a tumor suppressor function for the lipid phosphatase inositol polyphosphate 4-phosphatase type II (INPP4B) has been described in breast and prostate cancers, with impact on PI3K signaling output. Given the importance of PI3K pathway activity for melanoma formation and growth, we aimed to assess the role of INPP4B in melanocytic tumors. Our studies in native tumors suggest that decreased INPP4B expression is an event correlating with tumor progression in melanocytic neoplasms. We further demonstrate that INPP4B regulates PI3K/Akt signaling and exerts a tumor suppressor effect, impacting the proliferative, invasive, and tumorigenic capacity of melanoma cells. INPP4B expression in melanocytic neoplasms may therefore have potential as a biomarker for disease progression and as a modulator for the prediction of treatment outcome.

PMID:
24288008
DOI:
10.1038/jid.2013.511
[Indexed for MEDLINE]
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