Immune activated B cells are dominant in Prostate cancer - BCR sequencing
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB53813 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9873890_1.fastq.gz | Fastqsanger.gz | |||
| ERR9873890_2.fastq.gz | Fastqsanger.gz | |||
| ERR9873891_1.fastq.gz | Fastqsanger.gz | |||
| ERR9873891_2.fastq.gz | Fastqsanger.gz | |||
| ERR9873892_1.fastq.gz | Fastqsanger.gz |
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Project description:B cell receptor (BCR) signaling is a key determinant of chronic lymphocytic leukemia (CLL) pathophysiology. CD49d, the alpha4 subunit of the very late antigen-4 (VLA-4) integrin, can be activated by BCR signals; however, its role in modulating BCR functionality remains unknown. We used mouse models and primary human CLL to address this aspect. We found CD49d being not only required for bone marrow infiltration in TCL1 transgenic mice but also shaping human bone marrow infiltration patterns, along with patient outcome. In mice transplanted with TCL1 transgenic cells, CD49d loss altered leukemic cell localization in splenic niches. CD49d-deficient murine cells and human CD49d-low CLL cells could not form immune synapses to antigen-presenting membranes. CD49d-loss-related F-actin polymerization and transcriptomic defects in cytoskeleton-associated pathways were found in mouse and human. The requirement of CD49d for engraftment and actin organization could be recapitulated in a second murine model with highly aggressive transformed CLL. RNAseq analyses and kinome profiling revealed impaired antigen responsiveness due to kinase transcription and activity shifts in CD49d-deficient murine leukemic cells, recapitulated in human while applying several human BCR signatures. Finally, in human CLL expressing low CD49d, actin organization was deregulated, along with a desynchronization of Syk and PLCgamma activation. In summary, our findings establish CD49d as a key regulator of BCR functionality, linking integrin signaling to cytoskeletal dynamics and antigen responsiveness in CLL.
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Project description:Understanding the role of the immune microenvironment in modulating intratumor heterogeneity is essential for effective cancer therapies. Here we show that two types of tumor clonal landscapes emerge during early progression of prostate cancer in genetically-engineered mouse models. Using lineage tracing and single-cell transcriptomics, we find that slowly progressing tumors contain a multiclonal landscape of relatively homogenous subpopulations within a well-organized tumor microenvironment, whereas more advanced and aggressive tumors contain competing dominant and minor clones accompanied by a disordered microenvironment. We demonstrate that the dominant/minor modality is associated with differential immunoediting, in which minor clones are marked by increased expression of IFNγ-response genes and the T-cell activating chemokines Cxcl9 and Cxcl11. Furthermore, immunomodulation of the IFNγ pathway can rescue minor clones from elimination. These findings suggest new immunotherapy approaches to modulate clonal fitness and tumor progression in prostate cancer.
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Project description:Prostate cancer (PCa) is the second most common cancer in men. Diagnosis and risk assessment are widely based on serum Prostate Specific Antigen (PSA) and biopsy which have low accuracy. Towards the discovery of biomarkers for better patient stratification, we performed proteomic analysis of Formalin Fixed Paraffin Embedded (FFPE) prostate tissue specimens following optimized sample preparation protocol and LC-MS/MS. Comparative analysis of 86 PCa samples among grade groups 1-5 identified 301 differentially expressed proteins involved in metabolism, angiogenesis, response to stress and cytoskeleton organization. Additional analysis based on biochemical recurrence (BCR; BCR+ n=14, BCR- n=51) revealed 197 differentially expressed proteins that indicate disease persistence. Filtering the overlapping proteins of these analyses, seven proteins (NPM1, UQCRH, HSPA9, MRPL3, VCAN, SERBP1, HSPE1) had increased expression in advanced grades and in BCR+/BCR- and may play a critical role in PCa aggressiveness and persistence. Notably, our observations for NPM1, UQCRH and VCAN were validated in The Cancer Genome Atlas (TCGA), where they were upregulated in BCR+/BCR-. UQCRH levels were also associated with 5-year survival. Our study provides valuable insights on the key regulators of PCa progression and aggressiveness. The seven selected proteins could be used for the development of risk assessment tools.
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