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Embryonic stem cells (ESCs), which are susceptible to DNA damage, depend on a robust and highly efficient DNA damage response (DDR) mechanism for their survival. However, the implications of physical force-mediated DNA damage on ESC fate remain unclear. We show that stiffness-dependent spreading of mouse ESCs (mESCs) induces DNA damage through nuclear compression, with DNA damage causing differentiation through Lamin A/C. Interestingly, differentiation is associated with DNA damage and activation of the DDR factors such as ATR and CHK1. While ATR is typically known to play roles in DDR pathway, its role during stiffness-mediated nuclear compression and mESC differentiation is unknown. While our results show activation of CHK1 pathway and nuclear enrichment of activated ATR on stiff substrates, inhibiting ATR and CHK1 both result in reduction of Lamin A/C expression by different mechanisms. Overall, we demonstrate that mESC differentiation is driven by nuclear compression-mediated DNA damage and involves ATR-dependent modulation of Lamin A/C.
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http://dx.doi.org/10.1093/nar/gkaf852 | DOI Listing |
Leukemia
September 2025
Cleveland Clinic Research, Cleveland, OH, USA.
Hematopoietic malignancies (HM) represent the most common form of pediatric cancer with lymphoid malignancies being the predominant subtype in kids. The majority of lymphoid malignancies are proposed to occur sporadically with environmental, infectious and inflammatory triggers impacting oncogenesis in ways that are not yet fully understood. With the increased adoption of germline genetic testing in children with cancer, genetic predisposition to lymphoid malignancies is now recognized as an important aspect of clinical care and research.
View Article and Find Full Text PDFExp Neurobiol
August 2025
Institute of Medical Science, Ajou University School of Medicine, Suwon 16499, Korea.
Neural tumors represent diverse malignancies with distinct molecular profiles and present particular challenges due to the blood-brain barrier, heterogeneous molecular etiology including epigenetic dysregulation, and the affected organ's critical nature. KCC-07, a selective and blood-brain barrier penetrable MBD2 (methyl CpG binding domain protein 2) inhibitor, can suppress tumor development by inducing p53 signaling, proven only in medulloblastoma. Here we demonstrate KCC-07 treatment's application to other neural tumors.
View Article and Find Full Text PDFImmunol Cell Biol
September 2025
Department of Biotechnology, Indian Institute of Technology Hyderabad (IITH), Sangareddy, Telangana, India.
The immune system uses a variety of DNA sensors, including endo-lysosomal Toll-like receptors 9 (TLR9) and cytosolic DNA sensor cyclic GMP-AMP (cGAMP) synthase (cGAS). These sensors activate immune responses by inducing the production of a variety of cytokines, including type I interferons (IFN). Activation of cGAS requires DNA-cGAS interaction.
View Article and Find Full Text PDFChem Res Toxicol
September 2025
University of Texas Medical Branch, Galveston, Texas 77555, United States.
Glioblastoma (GBM) is a lethal brain tumor with limited therapeutic options. Temozolomide (TMZ), a standard-of-care chemotherapeutic agent, exerts its cytotoxicity by alkylating DNA, which triggers a DNA damage response and depletes ATP and NAD. However, TMZ also releases the byproduct 4-amino-5-imidazole carboxamide (AIC), which is believed to be a benign metabolite.
View Article and Find Full Text PDFInt J Biol Macromol
September 2025
Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi, 563000, Guizhou, China; The Public Experimental Center of Medicine, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi, 563000, Guizhou, China. Electronic address: kexixian@z
Chemotherapy resistance in lung adenocarcinoma (LUAD) limits clinical efficacy. In this study, we first established circ_IGF2BP1 knockdown models in LUAD cells (A549 and H1299). Using dual-luciferase reporter assays, functional analyses, and miR-885-3p rescue experiments, we demonstrated that circ_IGF2BP1 promotes LUAD cell proliferation, migration, and invasion by directly targeting miR-885-3p.
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