MINA controls proliferation and tumorigenesis of glioblastoma by epigenetically regulating cyclins and CDKs via H3K9me3 demethylation

• Published in: Oncogene Vol. 36; no. 3; pp. 387 - 396
• Main Authors: Huang, M-Y, Xuan, F, Liu, W, Cui, H-J
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 19.01.2017
• Subjects: Analysis; Animals; Brain Neoplasms - genetics; Brain Neoplasms - metabolism; Brain Neoplasms - pathology; Care and treatment; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Cyclin-Dependent Kinases - genetics; Cyclins - genetics; Diagnosis; Disease Progression; Epigenesis, Genetic; Epigenetics; Gene expression; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Genetic aspects; Glioblastoma - genetics; Glioblastoma - metabolism; Glioblastoma - pathology; Glioblastomas; Histones - metabolism; Humans; Kinases; Methylation; Mice; Neoplasm Transplantation; Nuclear Proteins - genetics; Nuclear Proteins - metabolism; Physiological aspects; Prognosis; Proliferating cell nuclear antigen; Studies; Survival Analysis; Transcription factors; Tumorigenesis; China

It is generally known that histone demethylases regulate gene transcription by altering the methylate status on histones, but their roles in cancers and the underlying molecular mechanisms still remain unclear. MYC-induced nuclear antigen (MINA) is reported to be a histone demethylase and highly exp...