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W. M. Gallagher, O. E. Bergin, M. Rafferty, Z. D. Kelly, I. M. Nolan, E. J. Fox, A. C. Culhane, L. McArdle, M. F. Fraga, L. Hughes, C. A. Currid, F. O’Mahony, A. Byrne, A. A. Murphy, C. Moss, S. McDonnell, R. L. Stallings, J. A. Plumb, M. Esteller, R. Brown, P. A. Dervan and D. J. Easty, “Multiple Markers for Melanoma Progression Re-gulated by Dna Methylation: Insights From Transcriptomic Studies,” Carcinogenesis, Vol. 26, No. 11, 2005, pp. 1856-1867.

has been cited by the following article:

• TITLE: Comparative Analysis of Protein Expression Concomitant with DNA Methyltransferase 3A Depletion in a Melanoma Cell Line

  AUTHORS: Xiaoyan Liu, Shengnan Tang, Tonghua Li, Haoyue Wang, Jiangming Sun, Qian Qiao, Jun Yao, Jian Fei

  KEYWORDS: Dnmt3a, Melanoma Cell Line, 1DE-LC-MS/MS; MAPK Signaling Pathway, Melanoma Pathway

  JOURNAL NAME: American Journal of Analytical Chemistry, Vol.2 No.5, September 22, 2011

  ABSTRACT: DNA methyltransferase 3A (Dnmt3a), a de novo methyltransferase, has attracted a great deal of attention for its important role played in tumorigenesis. We have previously demonstrated that melanoma is unable to grow in-vivo in conditions of Dnmt3a depletion in a mouse model. In this study, we cultured the Dnmt3a depletion B16 melanoma (Dnmt3a-D) cell line to conduct a comparative analysis of protein expression con-comitant with Dnmt3a depletion in a melanoma cell line. After two-dimensional separation, by gel electro-phoresis and liquid chromatography, combined with mass spectrometry analysis (1DE-LC-MS/MS), the re-sults demonstrated that 467 proteins were up-regulated and 535 proteins were down-regulated in the Dnmt3a-D cell line compared to the negative control (NC) cell line. The Genome Ontology (GO) and KEGG pathway were used to further analyze the altered proteins. KEGG pathway analysis indicated that the MAPK signaling pathway exhibited a greater alteration in proteins, an interesting finding due to the close relation-ship with tumorigenesis. The results strongly suggested that Dnmt3a potentially controls the process of tu-morigenesis through the regulation of the proteins (JNK1, p38α, ERK1, ERK2, and BRAF) involved in tu-mor-related pathways, such as the MAPK signaling pathway and melanoma pathway.