ArticleCell communication and signaling : CCS2024
Role of the CTCF/p300 axis in osteochondrogenic-like differentiation of polyploid giant cancer cells with daughter cells.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The influence of cell-cell fusion on cancer heterogeneity and its promise for targeted treatments.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Mechanisms of vascular calcification: cellular phenotype switching drives matrix remodeling and mineralized microenvironment formation.Frontiers in cardiovascular medicine · 2026Review
- p300: expanding beyond acetylation to mastermind lactylation-dependent tumorigenesis.Frontiers in cell and developmental biology · 2026Review
- Genomic Reshuffling After Cell Fusion: Catalyst for Cancer Evolution and Progression.Advances in experimental medicine and biology · 2026Review
- DEC1 regulates osteoblast proliferation and differentiation via the RUNX2 signaling pathway: Insights into the molecular mechanism of DEC1-mediated transcriptional regulation in bone metabolism.Open life sciences · 2026Article
- Modelling the monstrosities: experimental and computational systems for studying polyploid giant cancer cells.Expert reviews in molecular medicine · 2025Review
- Genomic structural equation modeling uncovers novel risk loci for bone metabolic disorders: cross-tissue genetic mechanisms and bone-brain axis regulation.BMC musculoskeletal disorders · 2025Article
- Polyploid giant cancer cells and tumor budding: translation from basic research to clinical application.Frontiers in oncology · 2025Review
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6 authors.
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Abstract
backgroundPolyploid giant cancer cells (PGCCs) have properties of cancer stem cells (CSCs). PGCCs with daughter cells (PDCs) undergo epithelial-mesenchymal transition and show enhanced cellular plasticity. This study aimed to elucidate the mechanisms underlying the osteo/chondrogenic-like differentiation of PDCs, which may be exploited therapeutically by transdifferentiation into post-mitotic and functional cells.
methodsCobalt chloride was used to induce PGCC formation in MDA-MB-231 and HEY cells, and PDCs were cultured in osteo/chondrogenic differentiation media. Alcian blue staining was used to confirm osteo/chondrogenic differentiation, and the cell cycle was detected using flow cytometry. The expression of osteo/chondrogenic differentiation-related proteins was compared, and a co-immunoprecipitation assay was used to demonstrate the interactions between proteins. Bioinformatic analysis was used to explore the regulatory mechanism of osteo/chondrogenic differentiation, and a dual-luciferase reporter assay was performed to validate the interaction between transcriptional factors and target genes. Animal xenograft models were used to confirm the osteo/chondrogenic differentiation of PDCs.
resultsWhen cultured in osteo/chondrogenic medium, the stemness of PDCs decreased, and the expression of osteo/chondrogenic-related markers increased. This osteo/chondrogenic-like process was regulated by the transforming growth factor-β pathway in a time-dependent manner. A concurrent increase in the expression of histone acetyltransferase p300 and the transcription factor CCCTC-binding factor (CTCF) was observed. Co-immunoprecipitation assays revealed that p300 acetylated the osteo/chondrogenic marker RUNT-related transcription factor 2 (RUNX2). Analysis of chromatin immunoprecipitation sequencing datasets revealed that both CTCF and histone H3 lysine 27 acetylation (H3K27ac) were enriched in the promoter region of E1A-associated protein p300 (P300). The four predicted binding sites for CTCF and P300 were validated using dual-luciferase reporter assays. We examined the interaction between CTCF and H3K27ac and found that these two proteins had a combined effect on the transactivation of P300.
conclusionCTCF, in synergy with H3K27ac, amplified the expression of P300, facilitating acetyl group transfer to RUNX2. This acetylation stabilized RUNX2 and promoted osteo/chondrogenic differentiation, thereby reducing the incidence of PDC malignancies.
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