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Hypoxia controls the glycobiological signature and related pro-tumorigenic properties of metastatic melanomas

ABSTRACT: Hypoxia controls the glycobiological signature and related pro-tumorigenic properties of metastatic melanomas

PROVIDER: PRJNA780950 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16959553.fastq.gz	Fastqsanger.gz
	SRR16959554.fastq.gz	Fastqsanger.gz
	SRR16959555.fastq.gz	Fastqsanger.gz
	SRR16959556.fastq.gz	Fastqsanger.gz
	SRR16959557.fastq.gz	Fastqsanger.gz

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Hypoxia controls the glycobiological signature and related pro-tumorigenic properties of metastatic melanomas

Project description:Metastatic melanoma (MM) has a five-year survival rate of only 37%. The major causes of MM-related mortality are distant organ involvement and treatment resistance. These metastatic activities are often potentiated by the persistence of tumor-initiating cells (TICs) thriving in areas of hypoxia. To enhance therapy success, it is, thus, critical to understand MM TIC properties and devise MM TIC-specific treatment strategies. Our recent data suggest that MM cells have a distinct MM glycome signature characterized by fetal i-linear poly-N-acetyllactosamines (poly-LacNAc) and loss of I-branching enzyme β1,6 N-acetylglucosaminyltransferase 2 (GCNT2) that promote tumorigenicity. Whether hypoxia can instruct MM TIC development by modulating the MM glycome signature remains unknown. Here, comparative analysis of GCNT2 levels on patient melanoma cells and clinical outcome confirmed the relationship between loss of GCNT2 and poor patient survival. Moreover, MM cells with low GCNT2 showed elevated TIC marker expression and increased TIC potential, in vivo. Under hypoxia, MM cells further lost GCNT2 and I-branched poly-LacNAc expression and showed corresponding elevations in TIC markers and other glycome-related alterations. Galectin (Gal)-8, notably, was upregulated under hypoxia, preferred binding to i-linear poly-LacNAcs, increased TIC marker CD271, and was significantly elevated in sera of melanoma patients. Knockdown of Gal-8 in MM cells significantly decreased CD271 levels, even under hypoxia. Results from this investigation reveal a key role for hypoxia in enforcing the MM glycome signature and for Gal-8 as a pro-tumorigenic lectin and putative biomarker of MM.

2022-08-03 | GSE188986 | GEO

Tumorigenic iPSC-NS/PCs with mesenchymal properties

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Mutant p53 elicits context-dependent pro-tumorigenic phenotypes

Project description:Mutant p53 elicits context-dependent pro-tumorigenic phenotypes

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Pro- and anti-tumorigenic capacity of immunoproteasomes in shaping the tumor microenvironment

Project description:Apart from the constitutive proteasome, the immunoproteasome that comprises the three proteolytic subunits LMP2, MECL-1 and LMP7 is expressed in most immune cells. In this study we describe two opposing roles for immunoproteasomes in regulating the tumor microenvironment. During chronic inflammation, immunoproteasomes modulated the expression of pro-tumorigenic cytokines and chemokines and enhanced infiltration of innate immune cells that led to the onset of colitis-associated carcinogenesies (CAC). In ulcerative colitis (UC) patients with high risk for CAC, immunoproteasome-induced pro-tumorigenic mediators were highly upregulated. Interestingly, the role for the same enzymatic complex in melanoma tumors is relatively unknown. We found that the high expression of immunoproteasomes in human melanoma was associated with better prognosis. Our data revealed that the immunoproteasome has a strong anti-tumorigenic function in cancer types with non-inflammatory microenvironment such as melanoma. CD8+ cytotoxic T lymphocytes (CTLs) from immunoproteasome-deficient mice were reduced during T cell homeostasis and were not able to combat melanoma efficiently. Our results indicate that the immunoproteasome exhibits either pro- or anti-tumoral properties in a context-dependent manner.

2021-08-18 | GSE150979 | GEO

Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (microarray)

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Aryl hydrocarbon receptor-interacting protein regulates tumorigenic and metastatic properties of colorectal cancer cells driving liver metastasis

Project description:Aryl hydrocarbon receptor-interacting protein (AIP), a putative positive intermediary in aryl hydrocarbon receptor-mediated signaling, is overexpressed in highly metastatic human KM12SM CRC cells, with high metastatic capacity to liver, and other highly metastatic CRC cells. Meta-analysis and immunohistochemistry were used to assess the relevance of this protein in CRC. Cellular functions and signaling mechanisms mediated by AIP were assessed by gain-of-function experiments and in vitro and in vivo experiments. A significant association of high AIP expression with poor CRC patients’ survival was observed. Gain-of-function and quantitative proteomics experiments demonstrated that AIP increased tumorigenic and metastatic properties of isogenic KM12C (poorly-metastatic) and KM12SM CRC cells. AIP overexpression dysregulated epithelial-to-mesenchymal (EMT) markers and induced several transcription factors and Cadherin-17 activation. The former induced the signaling activation of AKT, SRC, and JNK kinases to increase adhesion, migration and invasion of CRC cells. In vivo, AIP expressing KM12 cells induced tumor growth and liver metastasis. Furthermore, KM12C (poorly-metastatic) cells ectopically expressing AIP became metastatic to liver. Our data reveal new roles for AIP in regulating proteins associated with cancer and metastasis to induce tumorigenic and metastatic properties in colon cancer cells driving liver metastasis.

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RORc expressing immune cells negatively regulate tertiary lymphoid structure formation and support their pro-tumorigenic functions

Project description:Tertiary lymphoid structures (TLSs) are formed in many cancer types and have been correlated with better prognosis and response to immunotherapy. In liver cancer, TLSs have been reported to be pro-tumorigenic as they harbor tumor progenitor cells and nurture their growth. The processes involved in TLS development and acquisition of pro- or anti-tumorigenic phenotype in cancer are largely unknown. RORc expressing immune cells have been previously implicated in TLS formation, however we find that they are not necessary for TLS neogenesis in the context of liver inflammation. On the contrary, RORc expressing cells negatively regulate TLS formation, since in their absence TLSs form in excess. CD4 cells are essential for liver TLS formation whereas B cells are required for TLS formation specifically in the absence of RORc expressing cells. Importantly, in chronically inflamed livers lacking RORc expressing cells, TLSs become anti-tumorigenic, resulting in reduced tumor load. Comparing liver pro- and anti-tumorigenic TLSs by transcriptional, proteomic and immunohistochemical analyses, revealed enrichment of exhausted CD8 cells that retained effector functions as well as germinal center B cells and plasma cells in anti-tumorigenic TLSs. Cell depletion experiments revealed a role mainly for B cells in limiting tumor development, possibly via tumor directed antibodies. Thus, RORc expressing cells negatively regulate B cell responses, and facilitate the pro-tumorigenic functions of hepatic TLSs.

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Convergence of oncogenic and hormone receptor pathways promotes pro-metastatic phenotypes.

Project description:Cyclin D1b is a splice variant of the cell cycle regulator Cyclin D1 and is known to harbor divergent and highly oncogenic functions in human disease. While Cyclin D1b is induced during disease progression in many cancer types, the mechanisms underlying Cyclin D1b function remain poorly understood. Herein, models of human disease were utilized to resolve the downstream pathways requisite for the pro-tumorigenic functions of Cyclin D1b. Specifically, it was shown that Cyclin D1b modulates the expression of a large transcriptional network that cooperates with AR signaling to enhance tumor cell growth and invasive potential. Notably, Cyclin D1b promoted AR-dependent activation of genes associated with metastatic phenotypes. Further exploration determined that transcriptional induction of SNAI2 (Slug) was essential for Cyclin D1b- mediated proliferative and invasive properties, implicating Slug as a critical driver of disease progression. Importantly, Cyclin D1b expression highly correlated with that of Slug in clinical samples of advanced disease. Further, in vivo analyses provided strong evidence that Slug enhances both tumor growth and homing to distal soft tissues. Collectively, these findings reveal the underpinning mechanisms behind the pro-tumorigenic functions of Cyclin D1b, and demonstrate that the convergence of the Cyclin D1b-AR and Slug pathways results in the activation of processes critical for the promotion of lethal tumor phenotypes. Analysis of transcriptomes under the control of individual D-type cyclin isoforms in the hormone dependent prostate cancer cell line LNCaP in the presence and absence of androgen. LNCaP cells cultured in charcoal dextran treated media were transduced with virus encoding Cyclin D1a, Cyclin D1b, or control GFP for 24 hours in biological triplicate. Cells were then stimulated with either 1nM DHT or 0.01% EtOH (vehicle control) for 16 hours and harvested for RNA

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Eosinophils restrict CRC metastasis by inhibiting pro-tumorigenic Spp1+ macrophage differentiation.

Project description:Eosinophils restrict CRC metastasis by inhibiting pro-tumorigenic Spp1+ macrophage differentiation.

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