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Immunoediting instructs tumor metabolic reprogramming to support immune evasion [Bisulfite-seq]

ABSTRACT: Immunoediting sculpts immunogenicity and thwarts host anti-tumor responses in tumor cells during tumorigenesis; however, it remains unknown whether metabolic programming of tumor cells can be guided by immunosurveillance. Here, we report that T cell-mediated immunosurveillance in early staged tumorigenesis instructs c-Myc upregulation and metabolic reprogramming in tumor cells. This previously unexplored tumor-immune interaction is controlled by a non-canonical IFNg-STAT3 signaling and supports tumor immune evasion. Our findings uncover that immunoediting instructs deregulated bioenergetic programs in tumor cells for empowering them to disarm the T cell-mediated immunosurveillance by imposing metabolic tug-of-war between tumor and infiltrating T cells and forming the suppressive tumor microenvironment.

ORGANISM(S): Mus musculus

PROVIDER: GSE217481 | GEO | 2022/11/15

REPOSITORIES: GEO

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Immunoediting instructs tumor metabolic reprogramming to support immune evasion [smartseq]

Project description:Immunoediting sculpts immunogenicity and thwarts host anti-tumor responses in tumor cells during tumorigenesis; however, it remains unknown whether metabolic programming of tumor cells can be guided by immunosurveillance. Here, we report that T cell-mediated immunosurveillance in early staged tumorigenesis instructs c-Myc upregulation and metabolic reprogramming in tumor cells. This previously unexplored tumor-immune interaction is controlled by a non-canonical IFNg-STAT3 signaling and supports tumor immune evasion. Our findings uncover that immunoediting instructs deregulated bioenergetic programs in tumor cells for empowering them to disarm the T cell-mediated immunosurveillance by imposing metabolic tug-of-war between tumor and infiltrating T cells and forming the suppressive tumor microenvironment.

2022-11-15 | GSE217862 | GEO

Immunoediting instructs tumor metabolic reprogramming to support immune evasion [CRISPR-screen]

2022-11-15 | GSE217859 | GEO

Immunoediting instructs tumor metabolic reprogramming to support immune evasion [RNA-seq]

2022-11-15 | GSE217480 | GEO

Immunoediting instructs tumor metabolic reprogramming to support immune evasion [ExomeSeq]

2022-11-15 | GSE217479 | GEO

Immunoediting instructs tumor metabolic reprogramming to support immune evasion [ATAC-seq]

2022-11-15 | GSE217475 | GEO

Immunoediting instructs tumor metabolic reprogramming to support immune evasion [TCR-seq]

2022-11-15 | GSE217861 | GEO

Expression data transgenic mouse mammary tumors

Project description:Immunosurveillance constitutes the first step of cancer immunoediting in which developing malignant lesions are eliminated by anti-tumorigenic immune cells. However, the mechanisms by which neoplastic cells induce an immunosuppressive state to evade the immune response are still unclear. The transcription factor Stat3 has been implicated in breast carcinogenesis and tumor immunosuppression in advanced disease, but its involvement in early disease development has not been established. Here, we genetically ablated Stat3 in the tumor epithelia of the inducible PyVmT mammary tumor model and found that Stat3-deficient mice recapitulated the three phases of immunoediting: elimination, equilibrium, and escape. Pathological analyses revealed that Stat3-deficient mice initially formed hyperplastic and early adenoma-like lesions that later completely regressed, thereby preventing the emergence of mammary tumors in the majority of animals. Furthermore, tumor regression was correlated with massive immune infiltration into the Stat3-deficient lesions, leading to their elimination. In a minority of animals, focal, non-metastatic Stat3-deficient mammary tumors escaped immunosurveillance after a long latency or equilibrium period. Taken together, our findings suggest that tumor epithelial expression of Stat3 plays a critical role in promoting an immunosuppressive tumor microenvironment during breast tumor initiation and progression, and prompt further investigation of Stat3 inhibitory strategies that may reactivate the immunosurveillance program. We used microarrays to detail determine the transcriptional difference between PyVmT-driven mouse mammary tumors that progressed in the presence or absense of epithelial Stat3. Mammary tumors from transgenic mice were excise and flash frozen. Tumors were analyzed from 8 Stat3-proficient tumors and 6 Stat3-deficient tumors. RNA was extracted and hybridization on Affymetrix microarrays.

2015-11-25 | E-GEOD-75325 | biostudies-arrayexpress

Alvarez2019 - A nonlinear mathematical model of cell-mediated immune response for tumor phenotypic heterogeneity

Project description:This is a non-linear mathematical model of cancer immunosurveillance that takes into account intratumoral phenotypic heterogeneity, such as differential expression of cell surface receptors and growth factors, according to cell-mediated immune responses. The model describes phenomena that have also been observed in vivo, such as tumor dormancy, cancer immunoediting, and a strong sensitivity to initial conditions.

2019-08-12 | BIOMD0000000790 | BioModels

Expression data transgenic mouse mammary tumors

2015-11-25 | GSE75325 | GEO

PKCz restrains cancer cell transformation by inhibiting nutrient stress-induced metabolic reprogramming

Project description:Tumor cells utilize the so-called Warburg effect to allow for rapid proliferation with glucose as the main nutrient. We show here that, although PKCz is critical for that effect, its deficiency promotes the plasticity necessary for nutrient-stressed cancer cells to reprogram their metabolism to utilize glutamine through the serine biosynthetic pathway, empowering them to survive and proliferate in the absence of glucose. We show that PKCz deficiency enhances glutamine utilization and expression of two key enzymes of the pathway, PGHDGH and PSAT1, in cells cultured in the absence of glucose. The loss of PKCz in mice results in enhanced intestinal tumorigenesis and increased levels of these two metabolic enzymes, while patients with low levels of PKCz have a poor prognosis. Taken together, this suggests that PKCz is a critical metabolic tumor suppressor.

2013-01-01 | GSE42186 | GEO

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