ArticleMolecular cancer2021
CHEK1 and circCHEK1_246aa evoke chromosomal instability and induce bone lesion formation in multiple myeloma.
Article in Molecular cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 71 citations in OpenAlex.
- Integrative bioinformatics and machine learning reveal hub genes and immune signatures bridging type 2 diabetes mellitus, fracture susceptibility, and osteoblast differentiation dysfunction.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Matrine Suppresses Lung Cancer Progression via Dual Inhibition of CHEK1-Mediated DNA Damage Repair and PI3K/AKT Survival Signaling.Thoracic cancer · 2026Article
- NAT10-Mediated ac4C Modification of circANKRD12 Reprograms the Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Correction: CHEK1 and circCHEK1_246aa evoke chromosomal instability and induce bone lesion formation in multiple myeloma.Molecular cancer · 2026Article
- Dexamethasone activates anti-tumor immunity in multiple myeloma by dismantling the GR-PPP1CB complex to restore STING/IRF3 signaling.Journal for immunotherapy of cancer · 2026Article
- Pancancer Fine-Mapping of Mutational Intolerance Identifies CHEK1 as an Immunosuppressive Driver in Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multi-omics analysis and functional validation of CHEK1 as an independent prognostic biomarker in Pancreatic cancer.PloS one · 2026Article
- Identification and validation of biomarkers of Shenggu Zaizao Wan in the treatment of steroid-induced osteonecrosis of the femoral head by integrating network pharmacology and bulk transcriptomic.Frontiers in medicine · 2026Article
- Diagnostic significance of the checkpoint kinase 1 gene in high-grade gastroenteropancreatic neuroendocrine neoplasms.Experimental and therapeutic medicine · 2026Article
- Deciphering splicing heterogeneity at single-cell resolution by SCSES.Nature communications · 2025Article
- Extracellular vesicle-mediated delivery of circp53 suppresses the progression of multiple cancers by activating the CypD/TRAP/HSP90 pathway.Experimental & molecular medicine · 2025Article
- Development and validation of a multiple myeloma diagnostic model based on systemic lupus erythematosus-associated genes and identification of specific genes.Discover oncology · 2025Article
- Coding circular RNA in human cancer.Genes & diseases · 2025Review
- Differential changes in the microglial transcriptome between neonatal and adult mice after spinal cord injury.Scientific reports · 2025Article
- Bruceine A Inhibits Cell Proliferation by Targeting the USP13/PARP1 Signalling Pathway in Multiple Myeloma.Basic & clinical pharmacology & toxicology · 2025Article
- CICADA: a circRNA effort toward the ghost proteome.Nucleic acids research · 2025Article
- Article
- Immunoparesis in multiple myeloma: a current overview.Frontiers in oncology · 2025Review
- The Molecular Pathology of Blood Cancer: A Comprehensive Review of Chromosome and Genetic Abnormalities and Their Clinical Utility.British journal of biomedical science · 2025Review
- Circular RNA-Encoded Proteins in Disease Pathogenesis.International journal of biological sciences · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 6 institutions in 5 countries.
Funding
Abstract
backgroundMultiple myeloma (MM) is still incurable and characterized by clonal expansion of plasma cells in the bone marrow (BM). Therefore, effective therapeutic interventions must target both myeloma cells and the BM niche.
methodsCell proliferation, drug resistance, and chromosomal instability (CIN) induced by CHEK1 were confirmed by Giemsa staining, exon sequencing, immunofluorescence and xenograft model in vivo. Bone lesion was evaluated by Tartrate-resistant acid phosphatase (TRAP) staining. The existence of circCHEK1_246aa was evaluated by qPCR, Sanger sequencing and Mass Spectrometer.
resultsWe demonstrated that CHEK1 expression was significantly increased in human MM samples relative to normal plasma cells, and that in MM patients, high CHEK1 expression was associated with poor outcomes. Increased CHEK1 expression induced MM cellular proliferation and evoked drug-resistance in vitro and in vivo. CHEK1-mediated increases in cell proliferation and drug resistance were due in part to CHEK1-induced CIN. CHEK1 activated CIN, partly by phosphorylating CEP170. Interestingly, CHEK1 promoted osteoclast differentiation by upregulating NFATc1 expression. Intriguingly, we discovered that MM cells expressed circCHEK1_246aa, a circular CHEK1 RNA, which encoded and was translated to the CHEK1 kinase catalytic center. Transfection of circCHEK1_246aa increased MM CIN and osteoclast differentiation similarly to CHEK1 overexpression, suggesting that MM cells could secrete circCHEK1_246aa in the BM niche to increase the invasive potential of MM cells and promote osteoclast differentiation.
conclusionsOur findings suggest that targeting the enzymatic catalytic center encoded by CHEK1 mRNA and circCHEK1_246aa is a promising therapeutic modality to target both MM cells and BM niche.
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