Epigenetic silencing of JAM3 promotes esophageal cancer development by activating Wnt signaling

The role of JAM3 in different tumors is controversial. The epigenetic regulation and the mechanism of JAM3 remain to be elucidated in human esophageal cancer (EC). Eleven EC cell lines, 49 cases of esophageal intraepithelial neoplasia (EIN) and 760 cases of primary EC samples were employed. Methylat...

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Veröffentlicht in:	Clinical epigenetics 2022-12, Vol.14 (1), p.164, Article 164
Hauptverfasser:	Yang, Weili, Guo, Chao, Herman, James G, Zhu, Cheng, Lv, Honghui, Su, Xiaomo, Zhang, Lirong, Zhang, Meiying, Guo, Mingzhou
Format:	Artikel
Sprache:	eng
Schlagworte:	Analysis Animal models Animals Apoptosis Cell adhesion & migration Cell Adhesion Molecules - genetics Cell growth Cell migration Cell proliferation Cloning Decitabine DNA Methylation Efficiency Epigenesis, Genetic Epigenetic inheritance Epigenetics Esophageal cancer Esophageal Neoplasms - genetics Esophagus Humans Immunoglobulins Immunohistochemistry Methylation Mice Mutation Protein Processing, Post-Translational Roles Signal transduction Wnt protein Wnt Signaling Pathway Xenografts β-Catenin
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Zusammenfassung:	The role of JAM3 in different tumors is controversial. The epigenetic regulation and the mechanism of JAM3 remain to be elucidated in human esophageal cancer (EC). Eleven EC cell lines, 49 cases of esophageal intraepithelial neoplasia (EIN) and 760 cases of primary EC samples were employed. Methylation-specific polymerase chain reaction, immunohistochemistry, MTT, western blot and xenograft mouse models were applied in this study. The inverse association between RNA expression and promoter region methylation of JAM3 was found by analyzing 185 cases of EC samples extracted from the TCGA database (p
ISSN:	1868-7075 1868-7083 1868-7083 1868-7075
DOI:	10.1186/s13148-022-01388-3