ve-821 and Osteosarcoma

ve-821 has been researched along with Osteosarcoma* in 2 studies

Other Studies

2 other study(ies) available for ve-821 and Osteosarcoma

ArticleYear
High linear energy transfer carbon-ion irradiation upregulates PD-L1 expression more significantly than X-rays in human osteosarcoma U2OS cells.
    Journal of radiation research, 2021, Sep-13, Volume: 62, Issue:5

    Programmed death ligand 1 (PD-L1) expression on the surface of cancer cells affects the efficacy of anti-PD-1/PD-L1 immune checkpoint therapy. However, the mechanism underlying PD-L1 expression in cancer cells is not fully understood, particularly after ionizing radiation (IR). Here, we examined the impact of high linear energy transfer (LET) carbon-ion irradiation on the expression of PD-L1 in human osteosarcoma U2OS cells. We found that the upregulation of PD-L1 expression after high LET carbon-ion irradiation was greater than that induced by X-rays at the same physical and relative biological effectiveness (RBE) dose, and that the upregulation of PD-L1 induced by high LET carbon-ion irradiation was predominantly dependent on ataxia telangiectasia and Rad3-related (ATR) kinase activity. Moreover, we showed that the downstream signaling, e.g. STAT1 phosphorylation and IRF1 expression, was upregulated to a greater extent after high LET carbon-ion irradiation than X-rays, and that IRF1 upregulation was also ATR dependent. Finally, to visualize PD-L1 molecules on the cell surface in 3D, we applied immunofluorescence-based super-resolution imaging. The three-dimensional structured illumination microscopy (3D-SIM) analyses revealed substantial increases in the number of presented PD-L1 molecules on the cell surface after high LET carbon-ion irradiation compared with X-ray irradiation.

    Topics: Ataxia Telangiectasia Mutated Proteins; B7-H1 Antigen; Bone Neoplasms; Cell Line, Tumor; Gene Expression Regulation, Neoplastic; Heavy Ion Radiotherapy; Humans; Imaging, Three-Dimensional; Interferon Regulatory Factor-1; Linear Energy Transfer; Morpholines; Neoplasm Proteins; Osteosarcoma; Phosphorylation; Protein Processing, Post-Translational; Pyrazines; Pyrones; RNA, Messenger; RNA, Neoplasm; STAT1 Transcription Factor; Sulfones; Up-Regulation; X-Rays

2021
Alternative lengthening of telomeres renders cancer cells hypersensitive to ATR inhibitors.
    Science (New York, N.Y.), 2015, Jan-16, Volume: 347, Issue:6219

    Cancer cells rely on telomerase or the alternative lengthening of telomeres (ALT) pathway to overcome replicative mortality. ALT is mediated by recombination and is prevalent in a subset of human cancers, yet whether it can be exploited therapeutically remains unknown. Loss of the chromatin-remodeling protein ATRX associates with ALT in cancers. Here, we show that ATRX loss compromises cell-cycle regulation of the telomeric noncoding RNA TERRA and leads to persistent association of replication protein A (RPA) with telomeres after DNA replication, creating a recombinogenic nucleoprotein structure. Inhibition of the protein kinase ATR, a critical regulator of recombination recruited by RPA, disrupts ALT and triggers chromosome fragmentation and apoptosis in ALT cells. The cell death induced by ATR inhibitors is highly selective for cancer cells that rely on ALT, suggesting that such inhibitors may be useful for treatment of ALT-positive cancers.

    Topics: Antineoplastic Agents; Apoptosis; Ataxia Telangiectasia Mutated Proteins; Cell Cycle; Cell Line, Tumor; DNA Helicases; Gene Knockdown Techniques; Glioma; HeLa Cells; Homologous Recombination; Humans; Nuclear Proteins; Osteosarcoma; Promyelocytic Leukemia Protein; Pyrazines; Replication Protein A; RNA, Untranslated; Sulfones; Telomerase; Telomere; Telomere Homeostasis; Telomeric Repeat Binding Protein 2; Transcription Factors; Tumor Suppressor Proteins; X-linked Nuclear Protein

2015
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