17 results on '"Chet Oon"'
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2. Supplementary Figures from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
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Mara H. Sherman, Sunil R. Hingorani, Zheng Xia, David W. Dawson, Rosemary Makar, Ariana Sattler, Jennifer M. Finan, Wesley Horton, Hannah Sanford-Crane, Sohinee Bhattacharyya, Chet Oon, M. Kathrina Onate, Duanchen Sun, Christopher C. DuFort, R. Crystal Chaw, Mark W. Berry, and Erin J. Helms
- Abstract
Figures S1-S3
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- 2023
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3. Table S2 from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
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Mara H. Sherman, Sunil R. Hingorani, Zheng Xia, David W. Dawson, Rosemary Makar, Ariana Sattler, Jennifer M. Finan, Wesley Horton, Hannah Sanford-Crane, Sohinee Bhattacharyya, Chet Oon, M. Kathrina Onate, Duanchen Sun, Christopher C. DuFort, R. Crystal Chaw, Mark W. Berry, and Erin J. Helms
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Table S2
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- 2023
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4. Table S1 from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
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Mara H. Sherman, Sunil R. Hingorani, Zheng Xia, David W. Dawson, Rosemary Makar, Ariana Sattler, Jennifer M. Finan, Wesley Horton, Hannah Sanford-Crane, Sohinee Bhattacharyya, Chet Oon, M. Kathrina Onate, Duanchen Sun, Christopher C. DuFort, R. Crystal Chaw, Mark W. Berry, and Erin J. Helms
- Abstract
Table S1
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- 2023
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5. Data from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity
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Mara H. Sherman, Peter Tontonoz, Lisa M. Coussens, Zheng Xia, Sohinee Bhattacharyya, Holly Sandborg, Luis Diaz, Shanthi Nagarajan, Duanchen Sun, Courtney B. Betts, Xu Xiao, Chet Oon, Hannah Sanford-Crane, and Jaime Abrego
- Abstract
Despite significant recent advances in precision medicine, pancreatic ductal adenocarcinoma (PDAC) remains near uniformly lethal. Although immune-modulatory therapies hold promise to meaningfully improve outcomes for patients with PDAC, the development of such therapies requires an improved understanding of the immune evasion mechanisms that characterize the PDAC microenvironment. Here, we show that cancer cell–intrinsic glutamic-oxaloacetic transaminase 2 (GOT2) shapes the immune microenvironment to suppress antitumor immunity. Mechanistically, we find that GOT2 functions beyond its established role in the malate–aspartate shuttle and promotes the transcriptional activity of nuclear receptor peroxisome proliferator–activated receptor delta (PPARδ), facilitated by direct fatty acid binding. Although GOT2 is dispensable for cancer cell proliferation in vivo, the GOT2–PPARδ axis promotes spatial restriction of both CD4+ and CD8+ T cells from the tumor microenvironment. Our results demonstrate a noncanonical function for an established mitochondrial enzyme in transcriptional regulation of immune evasion, which may be exploitable to promote a productive antitumor immune response.Significance:Prior studies demonstrate the important moonlighting functions of metabolic enzymes in cancer. We find that the mitochondrial transaminase GOT2 binds directly to fatty acid ligands that regulate the nuclear receptor PPARδ, and this functional interaction critically regulates the immune microenvironment of pancreatic cancer to promote tumor progression.See related commentary by Nwosu and di Magliano, p. 2237..This article is highlighted in the In This Issue feature, p. 2221
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- 2023
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6. Supplementary Methods from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
- Author
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Mara H. Sherman, Sunil R. Hingorani, Zheng Xia, David W. Dawson, Rosemary Makar, Ariana Sattler, Jennifer M. Finan, Wesley Horton, Hannah Sanford-Crane, Sohinee Bhattacharyya, Chet Oon, M. Kathrina Onate, Duanchen Sun, Christopher C. DuFort, R. Crystal Chaw, Mark W. Berry, and Erin J. Helms
- Abstract
Supplementary Methods
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- 2023
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7. Supplementary Methods from A Stromal Lysolipid–Autotaxin Signaling Axis Promotes Pancreatic Tumor Progression
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Mara H. Sherman, Jurre J. Kamphorst, Rosalie C. Sears, Jim C. Norman, Jennifer P. Morton, Craig Dorrell, Colin Nixon, Ronald M. Evans, Rosa F. Hwang, David Novo, Michelle Schug, Esmee Vringer, Nicholas D. Kendsersky, Jason Link, Brittany L. Allen-Petersen, Sergey Tumanov, Sohinee Bhattacharyya, Mark Berry, Jacqueline Tait-Mulder, Chet Oon, Vinay Bulusu, and Francesca R. Auciello
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Supplementary Methods
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- 2023
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8. Supplementary Figures from A Stromal Lysolipid–Autotaxin Signaling Axis Promotes Pancreatic Tumor Progression
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Mara H. Sherman, Jurre J. Kamphorst, Rosalie C. Sears, Jim C. Norman, Jennifer P. Morton, Craig Dorrell, Colin Nixon, Ronald M. Evans, Rosa F. Hwang, David Novo, Michelle Schug, Esmee Vringer, Nicholas D. Kendsersky, Jason Link, Brittany L. Allen-Petersen, Sergey Tumanov, Sohinee Bhattacharyya, Mark Berry, Jacqueline Tait-Mulder, Chet Oon, Vinay Bulusu, and Francesca R. Auciello
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Figure S1-S5 with legends
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- 2023
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9. Supplementary Table 1 from A Stromal Lysolipid–Autotaxin Signaling Axis Promotes Pancreatic Tumor Progression
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Mara H. Sherman, Jurre J. Kamphorst, Rosalie C. Sears, Jim C. Norman, Jennifer P. Morton, Craig Dorrell, Colin Nixon, Ronald M. Evans, Rosa F. Hwang, David Novo, Michelle Schug, Esmee Vringer, Nicholas D. Kendsersky, Jason Link, Brittany L. Allen-Petersen, Sergey Tumanov, Sohinee Bhattacharyya, Mark Berry, Jacqueline Tait-Mulder, Chet Oon, Vinay Bulusu, and Francesca R. Auciello
- Abstract
Table S1
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- 2023
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10. Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
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Hannah Sanford-Crane, Jennifer M. Finan, Mark W. Berry, Sohinee Bhattacharyya, Wesley Horton, Erin Helms, Christopher C. DuFort, Chet Oon, Zheng Xia, Rosemary Makar, R. Crystal Chaw, Ariana Sattler, David W. Dawson, Mara H. Sherman, Duanchen Sun, M. Kathrina Onate, and Sunil R. Hingorani
- Subjects
Male ,Stromal cell ,endocrine system diseases ,medicine.medical_treatment ,Population ,Biology ,Extracellular matrix ,Mice ,Cancer-Associated Fibroblasts ,Pancreatic cancer ,medicine ,Animals ,Humans ,education ,Tumor microenvironment ,education.field_of_study ,Growth factor ,Mesenchymal stem cell ,Mesenchymal Stem Cells ,medicine.disease ,digestive system diseases ,Gene Expression Regulation, Neoplastic ,Pancreatic Neoplasms ,Oncology ,Tumor progression ,Cancer research ,Female - Abstract
Cancer-associated fibroblast (CAF) heterogeneity is increasingly appreciated, but the origins and functions of distinct CAF subtypes remain poorly understood. The abundant and transcriptionally diverse CAF population in pancreatic ductal adenocarcinoma (PDAC) is thought to arise from a common cell of origin, pancreatic stellate cells (PSC), with diversification resulting from cytokine and growth factor gradients within the tumor microenvironment. Here we analyzed the differentiation and function of PSCs during tumor progression in vivo. Contrary to expectations, we found that PSCs give rise to a numerically minor subset of PDAC CAFs. Targeted ablation of PSC-derived CAFs within their host tissue revealed nonredundant functions for this defined CAF population in shaping the PDAC microenvironment, including production of specific extracellular matrix components and tissue stiffness regulation. Together, these findings link stromal evolution from distinct cells of origin to transcriptional heterogeneity among PDAC CAFs and demonstrate unique functions for CAFs of a defined cellular origin. Significance: By tracking and ablating a specific CAF population, we find that a numerically minor CAF subtype from a defined cell of origin plays unique roles in establishing the pancreatic tumor microenvironment. Together with prior studies, this work suggests that mesenchymal lineage heterogeneity and signaling gradients diversify PDAC CAFs. See related commentary by Cukierman, p. 296. This article is highlighted in the In This Issue feature, p. 275
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- 2021
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11. A cancer cell-intrinsic GOT2-PPARδ axis suppresses antitumor immunity
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Jaime Abrego, Hannah Sanford-Crane, Chet Oon, Xu Xiao, Courtney B. Betts, Duanchen Sun, Shanthi Nagarajan, Luis Diaz, Holly Sandborg, Sohinee Bhattacharyya, Zheng Xia, Lisa M. Coussens, Peter Tontonoz, and Mara H. Sherman
- Subjects
Immunosuppression Therapy ,Aspartic Acid ,Inflammatory and immune system ,Carcinoma ,Oncology and Carcinogenesis ,Fatty Acids ,Malates ,Ligands ,Article ,Pancreatic Neoplasms ,Pancreatic Cancer ,Rare Diseases ,Oncology ,Pancreatic Ductal ,Tumor Microenvironment ,2.1 Biological and endogenous factors ,Humans ,Aspartate Aminotransferases ,PPAR delta ,Aetiology ,Digestive Diseases ,Carcinoma, Pancreatic Ductal ,Cancer ,Aspartate Aminotransferase, Mitochondrial - Abstract
Despite significant recent advances in precision medicine, pancreatic ductal adenocarcinoma (PDAC) remains near uniformly lethal. Although immune-modulatory therapies hold promise to meaningfully improve outcomes for patients with PDAC, the development of such therapies requires an improved understanding of the immune evasion mechanisms that characterize the PDAC microenvironment. Here, we show that cancer cell–intrinsic glutamic-oxaloacetic transaminase 2 (GOT2) shapes the immune microenvironment to suppress antitumor immunity. Mechanistically, we find that GOT2 functions beyond its established role in the malate–aspartate shuttle and promotes the transcriptional activity of nuclear receptor peroxisome proliferator–activated receptor delta (PPARδ), facilitated by direct fatty acid binding. Although GOT2 is dispensable for cancer cell proliferation in vivo, the GOT2–PPARδ axis promotes spatial restriction of both CD4+ and CD8+ T cells from the tumor microenvironment. Our results demonstrate a noncanonical function for an established mitochondrial enzyme in transcriptional regulation of immune evasion, which may be exploitable to promote a productive antitumor immune response. Significance: Prior studies demonstrate the important moonlighting functions of metabolic enzymes in cancer. We find that the mitochondrial transaminase GOT2 binds directly to fatty acid ligands that regulate the nuclear receptor PPARδ, and this functional interaction critically regulates the immune microenvironment of pancreatic cancer to promote tumor progression. See related commentary by Nwosu and di Magliano, p. 2237.. This article is highlighted in the In This Issue feature, p. 2221
- Published
- 2022
12. MitoSOX Green for Visualizing Superoxide in Mitochondria
- Author
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Jongtae Yang, Bhaskar Mandavilli, Breanna Mohr, Chet Oon, and Sarah Youngblood
- Subjects
Physiology (medical) ,Biochemistry - Published
- 2022
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13. A Stromal Lysolipid–Autotaxin Signaling Axis Promotes Pancreatic Tumor Progression
- Author
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Jennifer P. Morton, Craig Dorrell, Jason Link, Francesca R. Auciello, Jacqueline Tait-Mulder, Rosa F. Hwang, Colin Nixon, David Novo, Mara H. Sherman, Nicholas D. Kendsersky, Jim C. Norman, Sergey Tumanov, Ronald M. Evans, Michelle Schug, Sohinee Bhattacharyya, Chet Oon, Esmee Vringer, Brittany L. Allen-Petersen, Mark W. Berry, Rosalie C. Sears, Jurre J. Kamphorst, and Vinay Bulusu
- Subjects
Male ,0301 basic medicine ,Stromal cell ,endocrine system diseases ,Mice, Nude ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Cell Movement ,Lysophosphatidic acid ,Tumor Cells, Cultured ,Animals ,Humans ,Protein kinase B ,Cell Proliferation ,Phosphoric Diester Hydrolases ,Chemistry ,Cell growth ,Pancreatic Stellate Cells ,Transdifferentiation ,Lysophosphatidylcholines ,Xenograft Model Antitumor Assays ,digestive system diseases ,Mice, Inbred C57BL ,Pancreatic Neoplasms ,Disease Models, Animal ,030104 developmental biology ,Oncology ,030220 oncology & carcinogenesis ,Disease Progression ,Hepatic stellate cell ,Cancer research ,Female ,lipids (amino acids, peptides, and proteins) ,Stromal Cells ,Autotaxin ,Signal transduction ,Carcinoma, Pancreatic Ductal ,Signal Transduction - Abstract
Pancreatic ductal adenocarcinoma (PDAC) develops a pronounced stromal response reflecting an aberrant wound-healing process. This stromal reaction features transdifferentiation of tissue-resident pancreatic stellate cells (PSC) into activated cancer-associated fibroblasts, a process induced by PDAC cells but of unclear significance for PDAC progression. Here, we show that PSCs undergo a dramatic lipid metabolic shift during differentiation in the context of pancreatic tumorigenesis, including remodeling of the intracellular lipidome and secretion of abundant lipids in the activated, fibroblastic state. Specifically, stroma-derived lysophosphatidylcholines support PDAC cell synthesis of phosphatidylcholines, key components of cell membranes, and also facilitate production of the potent wound-healing mediator lysophosphatidic acid (LPA) by the extracellular enzyme autotaxin, which is overexpressed in PDAC. The autotaxin–LPA axis promotes PDAC cell proliferation, migration, and AKT activation, and genetic or pharmacologic autotaxin inhibition suppresses PDAC growth in vivo. Our work demonstrates how PDAC cells exploit the local production of wound-healing mediators to stimulate their own growth and migration. Significance: Our work highlights an unanticipated role for PSCs in producing the oncogenic LPA signaling lipid and demonstrates how PDAC tumor cells co-opt the release of wound-healing mediators by neighboring PSCs to promote their own proliferation and migration. See related commentary by Biffi and Tuveson, p. 578. This article is highlighted in the In This Issue feature, p. 565
- Published
- 2019
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14. Mesenchymal Lineage Heterogeneity Underlies Non-Redundant Functions of Pancreatic Cancer-Associated Fibroblasts
- Author
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Erin Helms, Rosemary Makar, Sunil R. Hingorani, Zheng Xia, Duanchen Sun, R. Crystal Chaw, Jennifer M. Finan, Christopher C. DuFort, Ariana Sattler, Chet Oon, Sohinee Bhattacharyya, Mara H. Sherman, Wesley Horton, Hannah Sanford-Crane, David W. Dawson, M. Kathrina Onate, and Mark W. Berry
- Subjects
Tumor microenvironment ,education.field_of_study ,Stromal cell ,Mesenchymal stem cell ,Population ,Biology ,medicine.disease ,Extracellular matrix ,Pancreatic tumor ,Tumor progression ,Pancreatic cancer ,Cancer research ,medicine ,education - Abstract
Cancer-associated fibroblast (CAF) heterogeneity is increasingly appreciated, but the origins and functions of distinct CAF subtypes remain poorly understood. The abundant and transcriptionally diverse CAF population in pancreatic ductal adenocarcinoma (PDAC) is thought to arise from a common cell of origin, pancreatic stellate cells (PSCs), with diversification resulting from cytokine and growth factor gradients within the tumor microenvironment. Here we analyzed the differentiation and function of PSCs during tumor progression in vivo. Contrary to expectations, we found that PSCs give rise to a numerically minor subset of PDAC CAFs. Targeted ablation of PSC-derived CAFs within their host tissue revealed non-redundant functions for this defined CAF population in shaping the PDAC microenvironment, including production of specific components of the extracellular matrix. Together, these findings link stromal evolution from distinct cells of origin to transcriptional heterogeneity among PDAC CAFs, and demonstrate unique functions for CAFs of a defined cellular origin.Statement of significanceBy tracking and ablating a specific CAF population, we find that a numerically minor CAF subtype from a defined cell of origin plays unique roles in establishing the pancreatic tumor microenvironment. Together with prior studies, this work suggests that mesenchymal lineage heterogeneity as well as signaling gradients diversify PDAC CAFs.
- Published
- 2021
- Full Text
- View/download PDF
15. A cancer cell-intrinsic GOT2-PPARδ axis suppresses antitumor immunity
- Author
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Sohinee Bhattacharyya, Peter Tontonoz, Xu Xiao, Mara H. Sherman, Hannah Sanford-Crane, Jaime Abrego, Shanthi Nagarajan, and Chet Oon
- Subjects
Tumor microenvironment ,Myeloid ,medicine.anatomical_structure ,Immune system ,Fatty acid binding ,Cancer cell ,medicine ,Cancer research ,Cancer ,Context (language use) ,Biology ,medicine.disease ,CD8 - Abstract
Despite significant recent advances in precision medicine1,2, pancreatic ductal adenocarcinoma (PDAC) remains near-uniformly lethal. While the most frequent genomic alterations in PDAC are not presently druggable3and conventional therapies are often ineffective in this disease4, immune-modulatory therapies hold promise to meaningfully improve outcomes for PDAC patients. Development of such therapies requires an improved understanding of the immune evasion mechanisms that characterize the PDAC microenvironment, including frequent exclusion of antineoplastic T cells and abundance of immune-suppressive myeloid cells5–9. Here we show that cancer cell-intrinsic glutamic-oxaloacetic transaminase 2 (GOT2) shapes the immune microenvironment to suppress antitumor immunity. Mechanistically, we find that GOT2 functions beyond its established role in the malate-aspartate shuttle10–13and promotes the transcriptional activity of nuclear receptor peroxisome proliferator-activated receptor delta (PPARδ), facilitated by direct fatty acid binding. While GOT2 in PDAC cells is dispensable for cancer cell proliferationin vivo, GOT2 loss results in T cell-dependent suppression of tumor growth, and genetic or pharmacologic activation of PPARδ restores PDAC progression in the GOT2-null context. This cancer cell-intrinsic GOT2-PPARδ axis promotes spatial restriction of both CD4+and CD8+T cells from the tumor microenvironment, and fosters the immune-suppressive phenotype of tumor-infiltrating myeloid cells. Our results demonstrate a non-canonical function for an established mitochondrial enzyme in transcriptional regulation of immune evasion, which may be exploitable to promote a productive antitumor immune response.
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- 2020
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16. Acidic fibroblast growth factor underlies microenvironmental regulation of MYC in pancreatic cancer
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Aayush Kothari, Jason Link, Rosalie C. Sears, Chet Oon, Wesley Horton, Sohinee Bhattacharyya, and Mara H. Sherman
- Subjects
0301 basic medicine ,Stromal cell ,Transcription, Genetic ,Immunology ,Regulator ,Paracrine Communication ,Biology ,medicine.disease_cause ,Proto-Oncogene Proteins c-myc ,03 medical and health sciences ,Paracrine signalling ,Mice ,0302 clinical medicine ,Cancer-Associated Fibroblasts ,Cell Line, Tumor ,medicine ,Tumor Microenvironment ,Immunology and Allergy ,Animals ,Humans ,Solid Tumors ,Protein kinase B ,Tumor microenvironment ,Glycogen Synthase Kinase 3 beta ,Brief Definitive Report ,FGF1 ,3. Good health ,Pancreatic Neoplasms ,030104 developmental biology ,030220 oncology & carcinogenesis ,Cancer research ,Fibroblast Growth Factor 1 ,KRAS ,Signal transduction ,Carcinogenesis ,Proto-Oncogene Proteins c-akt ,Signal Transduction - Abstract
Here Bhattacharyya et al. show that MYC is a molecular point of convergence for microenvironmental and cell-autonomous signals in RAS-transformed pancreatic cancer cells. They identify cancer-associated fibroblast–derived FGF1 as a critical paracrine regulator of MYC, and a novel link between the pancreatic tumor microenvironment and oncogenic transcription., Despite a critical role for MYC as an effector of oncogenic RAS, strategies to target MYC activity in RAS-driven cancers are lacking. In genetically engineered mouse models of lung and pancreatic cancer, oncogenic KRAS is insufficient to drive tumorigenesis, while addition of modest MYC overexpression drives robust tumor formation, suggesting that mechanisms beyond the RAS pathway play key roles in MYC regulation and RAS-driven tumorigenesis. Here we show that acidic fibroblast growth factor (FGF1) derived from cancer-associated fibroblasts (CAFs) cooperates with cancer cell–autonomous signals to increase MYC level, promoter occupancy, and activity. FGF1 is necessary and sufficient for paracrine regulation of MYC protein stability, signaling through AKT and GSK-3β to increase MYC half-life. Patient specimens reveal a strong correlation between stromal CAF content and MYC protein level in the neoplastic compartment, and identify CAFs as the specific source of FGF1 in the tumor microenvironment. Together, our findings demonstrate that MYC is coordinately regulated by cell-autonomous and microenvironmental signals, and establish CAF-derived FGF1 as a novel paracrine regulator of oncogenic transcription.
- Published
- 2020
17. Abstract PO-095: A cancer cell-intrinsic GOT2-PPARδ axis suppresses antitumor immunity
- Author
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Duanchen Sun, Mara H. Sherman, Shanthi Nagarajan, Courtney Betts, Lisa M. Coussens, Jaime Abrego, Zheng Xia, Xu Xiao, Chet Oon, Peter Tontonoz, and Hannah Sanford-Crane
- Subjects
Cancer Research ,Chemistry ,Wild type ,medicine.disease_cause ,Acquired immune system ,Cell biology ,Immune system ,Oncology ,Cell culture ,Cancer cell ,medicine ,Receptor ,Carcinogenesis ,Transcription factor - Abstract
Glutamic-oxaloacetic transaminase 2 (GOT2) encodes a product with dual functions: primarily as a metabolic enzyme in mitochondria but also as a putative fatty acid (FA) binding protein. The purpose of this study is to investigate GOT2 function and FA-binding in PDA carcinogenesis. Depletion of GOT2 expression with CRISPR-Cas9 or shRNA in human and murine PDA cell lines shows no proliferation defects in vitro. However, GOT2-depleted cells orthotopically implanted in immunocompetent hosts fail to form large tumors. Analysis of cancer cell proliferation shows no difference between control and knockout (KO) tumors, indicating proliferation is not affected by GOT2 in vivo. Genes negatively correlated with GOT2 expression in human PDA reveal ontology clusters associated with adaptive immune response, which suggests an immune-modulatory role of GOT2. Quantitation of immune markers using conventional and multiplex immunohistochemistry confirmed enhanced immune cell infiltration in KO tumors. Inhibition of T cells with blocking antibodies rescued the growth of GOT2 KO tumors, further validating the role of GOT2 in mediating adaptive tumor immunity. In addition to its known mitochondrial and plasma membrane localization, GOT2 expression was observed in the nuclei of PDA cells. It was hypothesized that nuclear GOT2 can deliver FA-ligand to activate PPARs (peroxisome proliferator activator receptor), a class of ligand-activated transcription factors with tumor-promoting properties; specifically, the ubiquitously expressed PPARδ. Analysis of human PDA RNA-seq data shows a significant positive correlation between GOT2 and PPARδ target genes. GOT2-dependent PPARδ activation in PDA cells was confirmed in vitro. Computational modeling of the crystal structure of GOT2 revealed a suitable arachidonic acid (AA) docking site, a known PPARδ ligand. Lipid binding assays of purified protein confirmed direct GOT2-AA binding. The FA docking site of GOT2 was mutated and KO cells were reconstituted with wild type and mutant GOT2. GOT2 mutant cells, compared to wild-type GOT2 cells, showed reduced PPARδ activity, nuclear localization, and interaction with PPARδ. In vivo, mutant GOT2 increased immune cell infiltration. Lastly, the rescue of PPARδ activity in GOT2 KO tumors restores the formation of large tumors with similar immune microenvironments to control tumors. We conclude that the enzymatic function of GOT2 is dispensable for PDA proliferation. However, GOT2 direct FA binding enhances activation of PPARδ to promote an immune-suppressed microenvironment. This non-canonical function of GOT2 can be further explored to elucidate mechanisms of immune evasion in PDA and aid in the development of efficient immunotherapies to improve disease outcomes. Citation Format: Jaime Abrego, Hannah Sanford-Crane, Chet Oon, Xu Xiao, Courtney Betts, Duanchen Sun, Shanthi Nagarajan, Zheng Xia, Lisa Coussens, Peter Tontonoz, Mara Sherman. A cancer cell-intrinsic GOT2-PPARδ axis suppresses antitumor immunity [abstract]. In: Proceedings of the AACR Virtual Special Conference on Pancreatic Cancer; 2021 Sep 29-30. Philadelphia (PA): AACR; Cancer Res 2021;81(22 Suppl):Abstract nr PO-095.
- Published
- 2021
- Full Text
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