Gene expression profile at single cell level of conditional senescence in mouse Emu-myc B-cell lymphoma model
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE232445 | GEO | 2024/10/28
REPOSITORIES: GEO
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Project description:Treatment-induced senescence (TIS) is a DNA damage-triggered stress-response program, resulting in terminal arrest of affected cells. TIS plays an important role in cancer therapy, as many tumor cells would undergo TIS instead of apoptosis when exposed to standard chemotherapy regimens. The contribution of TIS to overall disease outcome is, however, unclear. To address this, we use lymphoma cells with conditional expression of the senescence-essential factor Suv39h1 (regulatable by 4-hydroxi-tamoxifen). Only cells with active Suv39h1 would undergo TIS in response to chemotherapy. Suv39h1 inactivation during the chemo-treatment would prevent TIS induction, while inactivation in fully senescent cells would allow outgrowth from the TIS cell cycle arrest. Such post-senescent cells (PS) show very different biological behavior than the cells growing in senescence-incompetent setting - never senescent (NS). The molecular characteristics of each of these treatment conditions are analyzed here by assessing global transcriptome data. We used global gene expression profiling by microarrays to gain insight in the molecular programme underlying the chemotherapy response in primary Emu-myc transgenic B-cell lymphomas.
2020-12-31 | GSE133860 | GEO
Project description:Oncogene-induced senescence (OIS), a terminal cell cycle block countering (pre)neoplastic lesions, is characterised on the molecular level by trimethylated histone H3 lysine 9 (h3K9me3), a transcriptionally repressive chromatin mark linked to silencing of S-phase-promoting genes. Whether H3K9-governed chromatin remodelling influences anticancer treatment-induced senescence (TIS) and whether functional control of this mark impacts on treatment outcome is not known. We used global gene expression profiling by microarrays to gain insight into the molecular responses of Emu-myc; Suv39h1-/- B-cell lymphoma cells to senescence-inducing anticancer agent Adriamycin (ADR). Primary lymphoma cells isolated from lymph nodes of Emu-Myc; Suv39h1-/- mice were used. In this model, the c-Myc oncogene is constitutively expressed in the cells of the B-cell lineage, leading to spontaneous development of aggressive B-cell lymphomas. Adriamycin (ADR), a cytostatic drug used as a standard part of several lymphoma treatment regimens, is known to massively induce TIS in Suv39h1-proficient lymphomas, protected from apoptosis by Bcl-2 over expression (Myc;Bcl2). In order to discern the impact of Suv39h1 to TIS induction under these conditions, we analysed here transcriptional profiles of matched pairs of Emu-myc;Suv39h1-/-;Bcl2 lymphomas, untreated or treated for 5 days with ADR.
2013-07-04 | E-GEOD-44355 | biostudies-arrayexpress
Project description:Oncogene-induced senescence (OIS), a terminal cell cycle block countering (pre)neoplastic lesions, is characterised on the molecular level by trimethylated histone H3 lysine 9 (h3K9me3), a transcriptionally repressive chromatin mark linked to silencing of S-phase-promoting genes. Whether H3K9-governed chromatin remodelling influences anticancer treatment-induced senescence (TIS) and whether functional control of this mark impacts on treatment outcome is not known. We used global gene expression profiling by microarrays to gain insight into the molecular responses of Emu-myc; Suv39h1-/- B-cell lymphoma cells to senescence-inducing anticancer agent Adriamycin (ADR).
2013-07-04 | GSE44355 | GEO
Project description:Treatment induced senescence (TIS) is a terminal cell cycle arrest program, increasingly recognized as a tumor suppressor mechanism complementing apoptosis in response to standard chemotherapy regimens. In particular cells with blocked apoptotic pathways rely on senescence as the only remaining failsafe mechanism to keep the neoplastic growth in check. However, little is known about biological properties, long-term fate of senescent tumor cells and their impact on the microenvironment. We used global gene expression profiling by microarrays to gain insight in the molecular programme underlying the treatment-induced senescence in Emu-myc transgenic B-cell lymphomas (apoptosis protected by Bcl2 overexpression), which robustly enter senescence in response to DNA-damaging anticancer agents such as Adriamycin (ADR).
2011-11-21 | GSE31099 | GEO
Project description:Treatment induced senescence (TIS) is a terminal cell cycle arrest program, increasingly recognized as a tumor suppressor mechanism complementing apoptosis in response to standard chemotherapy regimens. In particular cells with blocked apoptotic pathways rely on senescence as the only remaining failsafe mechanism to keep the neoplastic growth in check. However, little is known about biological properties, long-term fate of senescent tumor cells and their impact on the microenvironment. We used global gene expression profiling by microarrays to gain insight in the molecular programme underlying the treatment-induced senescence in Emu-myc transgenic B-cell lymphomas (apoptosis protected by Bcl2 overexpression), which robustly enter senescence in response to DNA-damaging anticancer agents such as Adriamycin (ADR).
2020-04-15 | GSE134753 | GEO
Project description:Treatment induced senescence (TIS) is a terminal cell cycle arrest program, increasingly recognized as a tumor suppressor mechanism complementing apoptosis in response to standard chemotherapy regimens. In particular cells with blocked apoptotic pathways rely on senescence as the only remaining failsafe mechanism to keep the neoplastic growth in check. However, little is known about biological properties, long-term fate of senescent tumor cells and their impact on the microenvironment. We used global gene expression profiling by microarrays to gain insight in the molecular programme underlying the treatment-induced senescence in Emu-myc transgenic B-cell lymphomas (apoptosis protected by Bcl2 overexpression), which robustly enter senescence in response to DNA-damaging anticancer agents such as Adriamycin (ADR). Primary lymphoma cells isolated from lymph nodes of Emu-Myc transgenic mice were used. In this model the the c-Myc oncogene is constitutively expressed in the cells of B-cell lineage, leading to spontaneous development of aggressive B-cell lymphomas, resembling Burkitt lymphoma in humans. In order to bring up the senescence as the main failsafe mechanism, primary lymphoma cells are protected from apoptosis by retroviral over-expression of a strong antiapoptotic protein Bcl2. These cells (Myc;Bcl2) massively undergo senescence upon DNA-damaging treatment. Adriamycin (ADR) is a cytostatic drug, used as a standard part of several lymphoma treatment regimens. In this study, transcriptional profiles of matched pairs of untreated vs. 5 days ADR treated Myc;Bcl2 lymphomas were analysed.
2011-11-21 | E-GEOD-31099 | biostudies-arrayexpress
Project description:Therapy-induced senescence (TIS) is a DNA damage-triggered irreversible cell-cycle block that terminates further expansion of (pre-)malignant lesions. Utilizing the Eµ-myc transgenic mouse lymphoma model (apoptosis protected by retroviral Bcl2-overexpression), we sought to elucidate the biological properties, long-term fate of senescent tumor cells and their impact on the microenvironment. We used global gene expression profiling by microarrays to gain insight into the molecular program underlying the treatment-induced senescence in Emu-myc transgenic B-cell lymphomas (apoptosis protected by Bcl2 overexpression), which robustly enter senescence in response to DNA-damaging anticancer agents such as Adriamycin (ADR).
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Project description:Expression data from senescence-inducible Suv39h1-ERT2 primary mouse Emu-myc B-cell lymphoma
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Project description:Here, we investigate therapy-induced senescence (TIS) as a reversible mechanism of drug resistance in breast cancer cells. High-dose doxorubicin treatment was used to induce TIS in four distinct breast cancer cell lines and the drug resistance/sensitivity pattern of parental and TIS cells were investigated using a panel of FDA-approved anticancer molecules.
Proteome analysis confirmed the presence of the Senescence-Associated Secretory Phenotype (SASP), altered spliceosomal activity and proteins with significant role in immune evasion.
2024-11-19 | PXD058028 | JPOST Repository
Project description:Cellular senescence is an important in vivo mechanism that prevents the propagation of damaged cells. However, the precise mechanism(s) regulating senescence are not well characterized. Here, we find that ITGB3 (integrin beta 3 or β3) is epigenetically regulated by the Polycomb protein CBX7. β3 expression accelerates the onset of senescence in human primary fibroblasts, by activating the TGFβ pathway in a cell autonomous and non-cell autonomous manner. β3 levels are dynamically increased during oncogeneinduced senescence (OIS) through CBX7 epigenetic regulation. DNA-damage and therapy-induced senescence (TIS) also induce β3 expression. In fact, downregulation of β3 levels override OIS and TIS, independently of its ligand-binding activity. Moreover, cilengitide, a αvβ3 antagonist, has the ability to block the SASP without affecting proliferation. Finally, we show an increase in β3 levels during aging in mice and humans. Altogether, our data show that integrin β3 subunit is a marker and regulator of senescence.
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