ArticleThe Journal of biological chemistry2012
58-kDa microspherule protein (MSP58) is novel Brahma-related gene 1 (BRG1)-associated protein that modulates p53/p21 senescence pathway.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Integrated multi-omics identifies MCRS1 as a causal hub linking aging, metabolic syndrome, and breast cancer progression.International journal of surgery (London, England) · 2026Article
- MCRS1 is associated with immunosuppressive microenvironments in pan-cancer and promotes hepatocellular carcinoma malignant phenotypes.Translational cancer research · 2025Article
- Thioparib inhibits homologous recombination repair, activates the type I IFN response, and overcomes olaparib resistance.EMBO molecular medicine · 2023Article
- A Cell Culture Chip with Transparent, Micropillar-Decorated Bottom for Live Cell Imaging and Screening of Breast Cancer Cells.Micromachines · 2022Article
- MCRS1 is essential for epiblast development during early mouse embryogenesis.Reproduction (Cambridge, England) · 2020Article
- Comprehensive Analysis of the Safety Profile of a Single-Stranded RNA Nano-Structure Adjuvant.Pharmaceutics · 2019Article
- Mps1 regulates spindle morphology through MCRS1 to promote chromosome alignment.Molecular biology of the cell · 2019Article
- Epigenetic Regulation of Organ Regeneration in Zebrafish.Journal of cardiovascular development and disease · 2018Review
- Epigenetic modifiers: activities in renal cell carcinoma.Nature reviews. Urology · 2018Review
- Article
- Loss of BRG1 induces CRC cell senescence by regulating p53/p21 pathway.Cell death & disease · 2017Article
- Brahma-related gene 1 induces apoptosis in a p53-dependent manner in human rheumatoid fibroblast-like synoviocyte MH7A.Medicine · 2016Article
- Expression of MCRS1 and MCRS2 and their correlation with serum carcinoembryonic antigen in colorectal cancer.Experimental and therapeutic medicine · 2016Article
- Chromatin Remodeling Factor Brg1 Supports the Early Maintenance and Late Responsiveness of Nestin-Lineage Adult Neural Stem and Progenitor Cells.Stem cells (Dayton, Ohio) · 2015Article
- The candidate oncogene (MCRS1) promotes the growth of human lung cancer cells via the miR-155-Rb1 pathway.Journal of experimental & clinical cancer research : CR · 2015Article
- Identification and characterization of nuclear and nucleolar localization signals in 58-kDa microspherule protein (MSP58).Journal of biomedical science · 2015Article
- SEPT12/SPAG4/LAMINB1 complexes are required for maintaining the integrity of the nuclear envelope in postmeiotic male germ cells.PloS one · 2015Article
- Article
- Increased expression of the 58-kD microspherule protein (MSP58) is correlated with poor prognosis in glioma patients.Medical oncology (Northwood, London, England) · 2013Article
- The novel interaction between microspherule protein Msp58 and ubiquitin E3 ligase EDD regulates cell cycle progression.Biochimica et biophysica acta · 2013Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nucleolar 58-kDa microspherule protein (MSP58) protein is a candidate oncogene implicated in modulating cellular proliferation and malignant transformation. In this study, we show that knocking down MSP58 expression caused aneuploidy and led to apoptosis, whereas ectopic expression of MSP58 regulated cell proliferation in a context-dependent manner. Specifically, ectopic expression of MSP58 in normal human IMR90 and Hs68 diploid fibroblasts, the H184B5F5/M10 mammary epithelial cell line, HT1080 fibrosarcoma cells, primary mouse embryonic fibroblasts, and immortalized NIH3T3 fibroblasts resulted in induction of premature senescence, an enlarged and flattened cellular morphology, and increased senescence-associated β-galactosidase activity. MSP58-driven senescence was strictly dependent on the presence of functional p53 as revealed by the fact that normal cells with p53 knockdown by specific shRNA or cells with a mutated or functionally impaired p53 pathway were effective in bypassing MSP58-induced senescence. At least two senescence mechanisms are induced by MSP58. First, MSP58 activates the DNA damage response and p53/p21 signaling pathways. Second, MSP58, p53, and the SWI/SNF chromatin-remodeling subunit Brahma-related gene 1 (BRG1) form a ternary complex on the p21 promoter and collaborate to activate p21. Additionally, MSP58 protein levels increased in cells undergoing replicative senescence and stress-induced senescence. Notably, the results of analyzing expression levels of MSP58 between tumors and matched normal tissues showed significant changes (both up- and down-regulation) in its expression in various types of tumors. Our findings highlight new aspects of MSP58 in modulating cellular senescence and suggest that MSP58 has both oncogenic and tumor-suppressive properties.
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