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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.

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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.

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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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