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Tumor Repopulating Cell Transcriptome reveals Specific Cell Surface Biomarkers and Signaling Pathways

ABSTRACT: Tumor Repopulating Cell Transcriptome reveals Specific Cell Surface Biomarkers and Signaling Pathways

PROVIDER: PRJNA541001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9007924.fastq.gz	Fastqsanger.gz
	SRR9007925.fastq.gz	Fastqsanger.gz
	SRR9007926.fastq.gz	Fastqsanger.gz
	SRR9007927.fastq.gz	Fastqsanger.gz

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Tumor Repopulating Cell Transcriptome reveals Specific Cell Surface Biomarkers and Signaling Pathways

Project description:Cancer metastasis is the most deadly stage in cancer progression. Despite significant efforts over the last few decades, it remains elusive why only a very small fraction of tumorigenic cancer cells is able to generate metastatic colonization. Recently, we have shown that mechanically selected tumor-repopulating cells (TRCs), a highly tumorigenic subpopulation of mouse melanoma cells, can grow in 3D soft fibrin gels. However, the novel cell surface biomarkers and gene regulatory features of TRCs remain largely unknown. Here, we utilized RNA-sequencing method that uses next-generation sequencing (NGS) techniques for whole transcriptome profiling to elucidate novel cell surface biomarkers and active gene regulatory features. RNA-sequencing data was utilized in DAVID for identification of differentially expressed clusters of genes, including cell adhesion cluster. This allowed us to identify novel cell surface biomarkers such as Col2a1, NCAM1, F11R, and Negr1. We have validated the expression of these genes by real-time qPCR. Among the biomarkers, expression level of Col2a1 was found to be low in TRCs but 20 fold higher compared to parental B16F1 cells, thus making the marker very specific for TRCs. Our immunofluorescence microcopy study also shows high expression of Col2a1 in TRCs compared with parental B16F1 cells. KEGG pathway analysis showed JAK/STAT pathway, hypoxia, and Akt3 pathway to be highly active in TRCs. In addition, aerobic glycolysis pathway was found to be very active, indicating a typical Warburg effect of highly tumorigenic cells. Together, our study revealed novel and specific biomarkers of melanoma TRCs and their cryptic cell signaling pathways. Future studies will uncover if perturbation of these pathways can successfully neutralize TRCs.

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Defining the cell surface proteomic landscape of multiple myeloma reveals immunotherapeutic strategies and biomarkers of drug resistance

Project description:The myeloma cell surface proteome (“surfaceome”) not only determines tumor interaction with the microenvironment but serves as an emerging arena for therapeutic development. Here, we use glycoprotein capture proteomics to first define surface markers most-enriched on myeloma when compared to B-cell malignancy models, revealing unexpected biological signatures unique to malignant plasma cells. We next integrate our proteomic dataset with existing transcriptome databases, nominating CCR10 and TXNDC11 as possible monotherapeutic targets and CD48 as a promising co-target for increasing avidity of BCMA-directed cellular therapies. We further identify potential biomarkers of resistance to proteasome inhibitors and lenalidomide including changes in CD53, EVI2B, CD10, and CD33. Comparison of short-term treatment with chronic resistance delineates large differences in surface proteome profile under each type of drug exposure. Finally, we develop a miniaturized version of the surface proteomics protocol and present the first surface proteomic profile of a primary plasma cell sample. Our dataset provides a unique resource to advance the biological, therapeutic, and diagnostic understanding of myeloma.

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Sub-populations in the mammary repopulating units

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