Functional integration of microRNAs into oncogenic and tumor suppressor pathways.
A large body of evidence has documented abnormal microRNA (miRNA) expression patterns in diverse human malignancies. Given that miRNA expression is tightly regulated during development and cellular differentiation, aberrant miRNA expression in cancer cells is likely to be in part a consequence of the loss of normal cellular identity that accompanies malignant transformation. Nevertheless, it is now clear that miRNAs function as critical effectors of several canonical oncogenic and tumor suppressor pathways, including those controlled by Myc and p53. Gain- and loss-of-function of these factors in cancer cells contributes to miRNA dysregulation, directly influencing neoplastic phenotypes including cellular proliferation and apoptosis.
Lotterman
Craig D
CD
McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Kent
Oliver A
OA
Mendell
Joshua T
JT
D011495:Histone-Lysine N-Methyltransferase; D006801:Humans; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D051788:Myeloid-Lymphoid Leukemia Protein / Q000235:genetics / Q000378:metabolism*; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism*; D015514:Oncogene Proteins, Fusion / Q000235:genetics / Q000378:metabolism*; D011494:Protein Kinases / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
C497422:KMT2A protein, human; D035683:MicroRNAs; D015514:Oncogene Proteins, Fusion; D016271:Proto-Oncogene Proteins c-myc; D016159:Tumor Suppressor Protein p53; D051788:Myeloid-Lymphoid Leukemia Protein; D011495:Histone-Lysine N-Methyltransferase; D011494:Protein Kinases