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Quiescent human glioblastoma cancer stem cells mediate tumor initiation, expansion, and recurrence following chemotherapy

ABSTRACT: Quiescent human glioblastoma cancer stem cells mediate tumor initiation, expansion, and recurrence following chemotherapy

PROVIDER: PRJNA785966 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17120001_1.fastq.gz	Fastqsanger.gz
	SRR17120001_2.fastq.gz	Fastqsanger.gz
	SRR17120002_1.fastq.gz	Fastqsanger.gz
	SRR17120002_2.fastq.gz	Fastqsanger.gz
	SRR17120003_1.fastq.gz	Fastqsanger.gz

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Quiescent human glioblastoma cancer stem cells mediate tumor initiation, expansion, and recurrence following chemotherapy

Project description:We performed single cell RNA sequencing with eight patient derived xenograft samples to identify quiescent cancer stem cells in glioblastoma. Additionally two samples treated with temozolomide was sequenced to examine the evolution of the cancer stem cells upon chemotherapeutics.

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Project description:Cancer stem cells (CSCs) are profoundly associated with refractory nature of cancer. A quiescent population of CSCs is responsible for tumorigenesis and chemoresistance in leukemia, whereas neither the presence nor clinical importance of the quiescent CSCs is clearly established in solid tumors. In colon cancer, LGR5 is regarded as a functional marker of CSCs, but heterogeneity among LGR5+ cells was not clearly defined. Here we stratified LGR5+ cells by single-cell gene expression analyses and revealed that a tumorigenic population of mouse LGR5+ cells resides in a quiescent state. We identified 23 signature genes that were uniquely expressed in the quiescent CSCs of mouse tumors, and found that 7 of them were also specifically expressed in a quiescent population of LGR5+ cells in human colon xenograft tumors. Among them, PROX1 was expressed in invasive fronts of colon tumors. PROX1 was induced by TCF1 (TCF7), and the TCF1-mediated PROX1 expression was responsible for not only the maintenance of quiescence but also chemoresistance of colon cancer organoids. Knockout of PROX1 in patient-derived xenograft tumors resulted in inhibition of tumor recurrence after chemotherapeutic treatment. Our data underscore the therapeutic importance of a quiescent CSC population in colon cancer.

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PROX1 mediates chemoresistance-associated recurrence via maintenance of quiescent colon cancer stem cells

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Project description:Hematopoietic stem cells (HSCs) are maintained in the quiescent state for protection from exhaustion by a number of self-renewal divisions. To understand the in vivo kinetics of quiescent HSCs, we analyzed the cell cycle of CD201+150+48-Lin-Kit+Sca-1+ cells after transplantation and during development and aging using fluorescent ubiquitination-based cell cycle indicator (Fucci) mice to distinguish HSCs at the G0, G1, and S/G2/M phases. The quiescent HSC population, representing a functional HSC pool, rapidly expanded by three weeks after transplantation and by three weeks of age in development and gradually accumulated in bone marrow with aging. Single-cell RNA-sequencing with flow cytometric index sorting suggested that high CD201 and Sca-1 expression levels and a low level of mitochondrial activity were associated with quiescent HSCs. A novel set of candidate quiescent genes in HSCs was also provided. This study implied that controlling quiescent HSCs is important for the in vivo expansion and maintenance of functional HSCs.

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