Myc: Maestro of MicroRNAs.

Genes Cancer

Howard Hughes Medical Institute and McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Published: June 2010

Hyperactivity of the Myc oncogenic transcription factor dramatically reprograms gene expression to facilitate cellular proliferation and tumorigenesis. To elicit these effects, Myc coordinates the activation and repression of an extensive network of protein-coding genes and, as has recently been appreciated, noncoding RNAs including microRNAs (miRNAs). Consistent with their ability to potently influence cancer phenotypes, the regulation of miRNAs by Myc affects virtually all aspects of the Myc oncogenic program, including proliferation, survival, metabolism, angiogenesis, and metastasis. This review will summarize the current understanding of the mechanisms underlying Myc-dependent transcriptional and posttranscriptional control of miRNAs and the resultant effects on tumorigenesis. As miRNAs are integral nodes in the transcriptional network controlled by Myc, modulating their activity represents a promising new approach for cancer therapy.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2946068PMC
http://dx.doi.org/10.1177/1947601910377491DOI Listing

Publication Analysis

Top Keywords

myc oncogenic
8
myc
6
myc maestro
4
maestro micrornas
4
micrornas hyperactivity
4
hyperactivity myc
4
oncogenic transcription
4
transcription factor
4
factor dramatically
4
dramatically reprograms
4

Similar Publications

The endonuclease activity of MCPIP1 controls the neoplastic transformation of epithelial cells via the c-Met/CD44 axis.

Cell Commun Signal

January 2025

Department of General Biochemistry, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.

The RNase activity of MCPIP1 is essential for regulating cellular homeostasis, proliferation, and tumorigenesis. Our study elucidates the effects of downregulation of MCPIP1 expression and an RNase-inactivating mutation (D141N) on normal epithelial kidney cells, indicating that MCPIP1 expression is a key factor that suppresses neoplastic transformation. We observed that either expression downregulation or mutation of MCPIP1 significantly increased its clonogenicity and altered the expression of cancer stem cell (CSC) markers and factors involved in epithelial-to-mesenchymal transition (EMT).

View Article and Find Full Text PDF

Osteoarthritis (OA), affecting > 500 million people worldwide, profoundly affects the quality of life and ability to work. The mitogen-activated protein kinase (MAPK) signaling pathway plays an essential role in OA. To address the lack of studies focused on synovial cells in OA, we evaluated the expression patterns and roles of the MAPK signaling pathway components in OA synovial tissues using bioinformatics.

View Article and Find Full Text PDF

Orphan nuclear receptor NR2E3 is a new molecular vulnerability in solid tumors by activating p53.

Cell Death Dis

January 2025

Center for Precision Medicine Research, Marshfield Clinic Research Institute, Marshfield Clinic Health System, Marshfield, WI, USA.

The orphan nuclear receptor NR2E3 has emerged as a potential tumor suppressor, yet its precise mechanisms in tumorigenesis require further investigation. Here, we demonstrate that the full-length protein isoform of NR2E3 instead of its short isoform activates wild-type p53 and is capable of rescuing certain p53 mutations in various cancer cell lines. Importantly, we observe a higher frequency of NR2E3 mutations in three solid tumors compared to the reference population, highlighting its potential significance in tumorigenesis.

View Article and Find Full Text PDF

Discovery of a potent PROTAC degrader for RNA demethylase FTO as antileukemic therapy.

Acta Pharm Sin B

December 2024

School of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou 310024, China.

The fat mass and obesity-associated protein (FTO) is an RNA demethylase required for catalytic demethylation of -methyladenosine (mA); it is highly expressed and functions as an oncogene in acute myeloid leukemia (AML). Currently, the overarching objective of targeting FTO is to precisely inhibit the catalytic activity. Meanwhile, whether FTO degradation also exerts antileukemic effects remains unknown.

View Article and Find Full Text PDF

Cadmium (Cd) is a widely available metal that has been found to have a role in causing nonalcoholic fatty liver disease (NAFLD). However, the detailed toxicological targets and mechanisms by which Cd causes NAFLD are unknown. Therefore, the present work aims to reveal the main targets of action, cellular processes, and molecular pathways by which cadmium causes NAFLD.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!