ArticleCell cycle (Georgetown, Tex.)2011
CREG1 enhances p16(INK4a) -induced cellular senescence.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Paediatric therapeutic development workshop on osteosarcoma.British journal of cancer · 2026Review
- Hepatocyte cellular repressor of E1A-stimulated genes 1 protects against acetaminophen-induced liver injury by promoting autophagy.Acta pharmacologica Sinica · 2025Article
- Novel roles for CREG1 in hematopoiesis revealed by single-cell RNA sequencing.Cell & bioscience · 2025Article
- Creg1 Regulates Erythroid Development via TGF-β/Smad2-Klf1 Axis in Zebrafish.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Single-cell genomics identifies distinct B1 cell developmental pathways and reveals aging-related changes in the B-cell receptor repertoire.Cell & bioscience · 2022Article
- Hepatocyte-specific deletion of cellular repressor of E1A-stimulated genes 1 exacerbates alcohol-induced liver injury by activating stress kinases.International journal of biological sciences · 2022Article
- CREG1 promotes lysosomal biogenesis and function.Autophagy · 2021Article
- Effects of CREG1 on Age-Associated Metabolic Phenotypes and Renal Senescence in Mice.International journal of molecular sciences · 2021Article
- The secreted inhibitor of invasive cell growth CREG1 is negatively regulated by cathepsin proteases.Cellular and molecular life sciences : CMLS · 2021Article
- A Study of Prognostic Factors in Young Patients With Non-HPV Oral Cancer in Central Europe.Pathology oncology research : POR · 2021Article
- DNA hypermethylation: A novel mechanism of CREG gene suppression and atherosclerogenic endothelial dysfunction.Redox biology · 2020Article
- The Structure and Biological Function of CREG.Frontiers in cell and developmental biology · 2018Review
- Dermokine contributes to epithelial-mesenchymal transition through increased activation of signal transducer and activator of transcription 3 in pancreatic cancer.Cancer science · 2017Article
- Article
- Comparison of growth-related traits and gene expression profiles between the offspring of neomale (XX) and normal male (XY) rainbow trout.Marine biotechnology (New York, N.Y.) · 2015Article
- Discovery of prognostic biomarkers for predicting lung cancer metastasis using microarray and survival data.BMC bioinformatics · 2015Article
- Osteosarcoma Genetics and Epigenetics: Emerging Biology and Candidate Therapies.Critical reviews in oncogenesis · 2015Review
- Drosophila melanogaster cellular repressor of E1A-stimulated genes is a lysosomal protein essential for fly development.Biochimica et biophysica acta · 2014Article
- Epigenetic alterations in osteosarcoma: promising targets.Molecular biology reports · 2014Review
- Integrated Analysis of Dysregulated miRNA-gene Expression in HMGA2-silenced Retinoblastoma Cells.Bioinformatics and biology insights · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cellular senescence is an irreversible growth arrest that is activated in normal cells upon shortening of telomere and other cellular stresses. Bypassing cellular senescence is a necessary step for cells to become immortal during oncogenic transformation. During the spontaneous immortalization of Li-Fraumeni Syndrome (LFS) fibroblasts, we found that CREG1 (Cellular Repressor of E1A-stimulated Genes 1) expression was decreased during immortalization and increased in senescence. Moreover, we found that repression of CREG1 expression occurs via an epigenetic mechanism, promoter DNA methylation. Ectopic expression of CREG1 in the immortal LFS cell lines decreases cell proliferation but does not directly induce senescence. We confirmed this in osteosarcoma and fibrosarcoma cancer cell lines, cancers commonly seen in Li-Fraumeni Syndrome. In addition, we found that p16 (INK4a) is also downregulated in immortal cells and that coexpression of CREG1 and p16 (INK4a) , an inhibitor of CDK4/6 and Rb phosphorylation, has a greater effect than either CREG1 and p16 (INK4a) alone to reduce cell growth, induce cell cycle arrest and cellular senescence in immortal LFS fibroblasts, osteosarcoma and fibrosarcoma cell lines. Moreover, cooperation of CREG1 and p16 (INK4a) inhibits the expression of cyclin A and cyclin B by inhibiting promoter activity thereby decreasing mRNA and protein levels; these proteins are required for S-phase entry and G2/M transition. In conclusion, this is the first evidence to demonstrate that CREG1 enhances p16 (INK4a) -induced senescence by transcriptional repression of cell cycle-regulated genes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.