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

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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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