Ribosomal protein L23 negatively regulates cellular apoptosis via the RPL23/Miz-1/c-Myc circuit in higher-risk myelodysplastic syndrome
Adult
Cyclin-Dependent Kinase Inhibitor p21
Male
Ribosomal Proteins
Transcriptional Activation
0301 basic medicine
Adolescent
Science
Kruppel-Like Transcription Factors
Apoptosis
Article
Proto-Oncogene Proteins c-myc
03 medical and health sciences
Humans
Promoter Regions, Genetic
Aged
Aged, 80 and over
0303 health sciences
Q
R
Cell Cycle Checkpoints
Middle Aged
Microarray Analysis
Gene Expression Regulation
Myelodysplastic Syndromes
Medicine
Female
Signal Transduction
DOI:
10.1038/s41598-017-02403-x
Publication Date:
2017-05-18T09:55:26Z
AUTHORS (7)
ABSTRACT
Ribosomal protein (RP) L23 is a negative regulator of cellular apoptosis, and RPL23 overexpression associated with abnormal apoptotic resistance in CD34+ cells derived from patients higher-risk myelodysplastic syndrome (MDS). However, the mechanism underlying RPL23-induced MDS poorly understood. In this study, we showed that reduced expression led to suppressed viability, increased apoptosis G1-S cell cycle arrest. Gene microarray analysis comparing RPL23-knockdown control identified an array differentially expressed genes, which, Miz-1, was upregulated transactivation inhibitors p15Ink4b p21Cip1, Miz-1's functional repressor, c-Myc, downregulated. Cells demonstrated consistently c-Myc decreased Miz-1 compared lower-risk patients. conclusion, Miz-1-dependent induction p21Cip1 depressed under conditions elevated expression, leading Because encoded by target gene RPL23/Miz-1/c-Myc regulatory circuit provides feedback loop links efficient c-Myc's function suppress Miz-1-induced Cdk thereby leads
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