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Phospho-proteomics tandem mass tag datasets from cells with CEP350 genetic alteration | Datasets Supporting: Tumor Suppressive Functions of CEP350 in Cutaneous Melanoma Cells
Signaling changes induced by haploinsufficient loss or over-expression of CEP350 by global phospho-serine/threonine profiling melanoma cells expressing oncogenic BRAF-V600E. Raw data produced by the Proteomics and Metabolomics Core Facility and data analysis performed by the Biostatistics and Bioinformatics Shared Resource at the H. Lee Moffitt Cancer Center & Research Institute.
Supplementary datasets and other information accompanying manuscript: Tumor Suppressive Functions of CEP350 in Cutaneous Melanoma Cells by Aziz Aiderus, Bin Fang, John M. Koomen and Michael B. Mann.
Abstract: We previously identified Cep350 as a novel melanoma haploinsufficient melanoma tumor suppressor gene using SB transposon-mediated mutagenesis to drive melanoma progression in Braf(V600E) mutant (SB|Braf) mice functionally demonstrated that the human CEP350 ortholog is a new melanoma tumor-suppressor gene in human cancer cell lines (Mann et al., Nature Genetics, 2015). Further dissection of the latent tumor suppressive functions of CEP350 in cutaneous melanoma cells is essential for understanding its role in melanoma imitation and progression. In this work, we investigated the role of the novel tumor suppressive functions of CEP350 in cutaneous melanoma cells using comparative informatics, molecular oncology, and proteomics approaches to demonstrate that CEP350 acts via altered cytoskeletal dynamics to contribute to BRAF-V600E driven melanoma.
Funding
Moffitt/American Cancer Society-Institutional Research Grant
History
Select an IC:
- CA - National Cancer Institute (NCI)
Is this associated with a publication?
- Yes
I confirm there is no human identifiable information in this dataset.
- Yes
