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Genome-wide CRISPR screening on cytotoxic T lymphocytes mediated cell killing independent of Casp3, Mlkl, and Bid

ABSTRACT: To gain insight into cytotoxic lymphocyte–mediated, Casp3, necroptosis, and Mitochondrial outer membrane permeabilization (MOMP) independent cancer cell death, we leveraged the a CTL–αCD3–P815 killing system and performed a genome-wide CRISPR screen. Cas9 expressing and Casp3-/-Mlkl-/-Bid-/- mouse mastocytoma P815 cells were first transduced with Brie gRNA library and subjected to cytotoxic T lymphocytes-mediated selection. Surviving cells were collected and sequenced to identify genes/gRNAs enriched following selection.

ORGANISM(S): Mus musculus

PROVIDER: GSE336305 | GEO | 2026/06/26

REPOSITORIES: GEO

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Genome-wide CRISPR screening on cytotoxic T lymphocytes mediated cell killing independent of Casp3

Project description:To gain insight into cytotoxic lymphocyte–mediated, Casp3-independent cancer cell death, we leveraged the a CTL–αCD3–P815 killing system and performed a genome-wide CRISPR screen. Cas9 expressing and Casp3-/- mouse mastocytoma P815 cells were first transduced with Brie gRNA library and subjected to cytotoxic T lymphocytes-mediated selection. Surviving cells were collected and sequenced to identify genes/gRNAs enriched following selection.

2026-06-26 | GSE336303 | GEO

RNA-sequencing in mouse mastocytoma cell line P815

Project description:We report the transcriptome sequencing results of the mouse mastocytoma cell line P815. After ESR1-specific shRNA vectors (SH) or the negative control vectors (NC) were transfected, the transcriptome in P815 after estrogen stimulation. We also detected the transcriptome of P815 cells after estrogen stimulation with the administration of estrogen receptor inhibitors Tamoxifen and ICI-182780.

2021-09-14 | GSE181773 | GEO

Genome-wide CRISPR screening on cytotoxic T lymphocytes mediated cell killing independent of Casp3, Mlkl, and Bid

Project description:Genome-wide CRISPR screening on cytotoxic T lymphocytes mediated cell killing independent of Casp3, Mlkl, and Bid

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RNA-sequencing in mouse mastocytoma cell line P815

Project description:RNA-sequencing in mouse mastocytoma cell line P815

| PRJNA753456 | ENA

Mitochondrial outer membrane integrity regulates a ubiquitin-dependent NF-kB inflammatory response

Project description:Mitochondria are often essential for apoptosis through mitochondrial outer membrane permeabilization (MOMP). This central event enables cytochrome c release leading to caspase activation and rapid cell death. Recently, MOMP has been shown to be inherently pro-inflammatory, for instance, causing mitochondrial DNA-dependent activation of cGAS-STING signalling. Alongside having emerging functions in health and disease, MOMP associated inflammation can also elicit anti-tumour immunity. Nonetheless, how MOMP triggers inflammation and how the cell counteracts this remain poorly defined. Here, we find that upon MOMP, mitochondria are ubiquitylated in a promiscuous manner targeting proteins localised to both inner and outer mitochondrial membranes. Mitochondrial ubiquitylation serves to recruit the essential adaptor molecule, NEMO, leading to activation of pro-inflammatory NF-kB signalling. We find that disruption of mitochondrial outer membrane integrity through different means leads to engagement of a similar pro-inflammatory signalling platform. Thus, mitochondrial integrity directly controls inflammation, whereby permeabilised mitochondria initiate NF-?B signalling. This may be important for the various pathophysiological functions of MOMP-associated inflammation.

2023-12-15 | PXD040192 | Pride

Transcription profiling of mouse CD8 T cells in response to P1A antigen expressing tumor cells or cells not expressing 1A antigen

Project description:Activation status of CD8 T cells in response to a tumor challenge. Although both natural killer (NK) cells and CD8 T cells are capable of anti-tumor responses, Recombinase Activating Gene (RAG)-deficient mice, which have a normal component of NK cells, are incapable of rejecting the P815 mastocytoma tumor. We established a model where monoclonal CD8 T cell reactivity was restricted to the tumor antigen (Ag) P1A expressed on the P815 mastocytoma. Reconstitution of the RAG-deficient mice with these (TCRP1A) T cells conferred resistance to tumor growth selectively for the P1A-expressing, but not for a P1A-negative variant of P815. Nevertheless, TCRP1A CD8 T cells were efficient and necessary to promote the NK cell dependent rejection of P1A-negative tumors when both P1A-positive and -negative tumors were present at the same site. Gene expression profiling in NK cells infiltrating the P1A-positive, as compared to the P1A-negative tumor, in mice transferred with TCRP1A CD8 T cells established their acquisition of an activated effector phenotype. Help from CD8 T cells was provided locally, as it did not induce activation of NK cells present in a P1A-negative variant at a distant site, nor the rejection of this variant. These results illustrate a mechanism by which, in the face of immunoselection / editing, the synergy between specific anti-tumor Ag T cells and NK cells can contribute to the elimination of tumor cells whether or not they express the tumor Ag. This mechanism appears ineffective, however, once tumor variants lacking the tumor Ag are separated from the wild-type tumor, as would be the case in tumor metastasis.

2007-12-01 | E-MEXP-1285 | biostudies-arrayexpress

Transcription profiling of mouse NK cells in presence/absence of activated CD8 T cells

Project description:we compare NK cells in presence of activated CD8 T cells or not. Although both natural killer (NK) cells and CD8 T cells are capable of anti-tumor responses, Recombinase Activating Gene (RAG)-deficient mice, which have a normal component of NK cells, are incapable of rejecting the P815 mastocytoma tumor. We established a model where monoclonal CD8 T cell reactivity was restricted to the tumor antigen (Ag) P1A expressed on the P815 mastocytoma. Reconstitution of the RAG-deficient mice with these (TCRP1A) T cells conferred resistance to tumor growth selectively for the P1A-expressing, but not for a P1A-negative variant of P815. Nevertheless, TCRP1A CD8 T cells were efficient and necessary to promote the NK cell dependent rejection of P1A-negative tumors when both P1A-positive and -negative tumors were present at the same site. Gene expression profiling in NK cells infiltrating the P1A-positive, as compared to the P1A-negative tumor, in mice transferred with TCRP1A CD8 T cells established their acquisition of an activated effector phenotype. Help from CD8 T cells was provided locally, as it did not induce activation of NK cells present in a P1A-negative variant at a distant site, nor the rejection of this variant. These results illustrate a mechanism by which, in the face of immunoselection / editing, the synergy between specific anti-tumor Ag T cells and NK cells can contribute to the elimination of tumor cells whether or not they express the tumor Ag. This mechanism appears ineffective, however, once tumor variants lacking the tumor Ag are separated from the wild-type tumor, as would be the case in tumor metastasis.

2007-11-01 | E-MEXP-1284 | biostudies-arrayexpress

Investigating the role of Bax/Bak as a driver of inflammation in aging

Project description:Senescent cells drive age-related tissue dysfunction partially via the induction of a chronic senescence-associated secretory phenotype (SASP). Mitochondria are major regulators of the SASP; however, the underlying mechanisms have not been elucidated. Mitochondria are often essential for apoptosis, a cell fate distinct from cellular senescence. During apoptosis, widespread mitochondrial outer membrane permeabilization (MOMP) commits a cell to die. Here, we find that MOMP occurring in a subset of mitochondria is a feature of cellular senescence. This process, called minority MOMP (miMOMP), depends on the formation of BAX and BAK macropores leading to the release of mitochondrial DNA (mtDNA) into the cytosol, which in turn activates the cGAS-STING pathway, a major regulator of the SASP. Importantly, we found that inhibition of MOMP in vivo decreases inflammatory markers and improves healthspan in aged mice. Our results reveal, unexpectedly, that apoptosis and senescence are regulated by similar mitochondrial-dependent mechanisms, and that sub-lethal mitochondrial apoptotic stress is a major driver of the SASP. We also provide proof-of-concept that inhibition of miMOMP-induced inflammation may be a new therapeutic avenue to improve healthspan.

2023-08-16 | GSE235225 | GEO

RNA-seq analysis of apoptotic HCT116 cells shows widespread mRNA decay and limited noncoding RNA decay.

Project description:Rapid and widespread mRNA decay is a previously unappreciated feature of apoptosis. Previous work showed that apoptotic mRNA decay depends on mitochondrial outer membrane permeabilization (MOMP) and the RNA-processing enzymes, TUT4, TUT7, and DIS3L2. Which RNAs are decayed, however, was not known. Here we present RNA-seq data of TRAIL-induced apoptosis in HCT116 cells showing global decay of mRNAs as well as polyadenylated noncoding RNAs, beginning at the 3’-end.

2018-05-01 | GSE104602 | GEO

Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death

Project description:Cancer cell metabolism is increasingly recognized as providing an exciting therapeutic opportunity. However, a drug that directly couples targeting of a metabolic dependency with the induction of cell death in cancer cells has largely remained elusive. Here we report that the drug-like small-molecule ironomycin reduces the mitochondrial iron load, resulting in the potent disruption of mitochondrial metabolism. Ironomycin promotes the recruitment and activation of BAX/BAK, but the resulting mitochondrial outer membrane permeabilization (MOMP) does not lead to potent activation of the apoptotic caspases, nor is the ensuing cell death prevented by inhibiting the previously established pathways of programmed cell death. Consistent with the fact that ironomycin and BH3 mimetics induce MOMP through independent nonredundant pathways, we find that ironomycin exhibits marked in vitro and in vivo synergy with venetoclax and overcomes venetoclax resistance in primary patient samples.

2022-10-01 | GSE186088 | GEO

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