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ABSTRACT: Glioblastoma quiescent cells hijack astrocyte-derived mitochondria to drive activation and malignancy

PROVIDER: PRJNA1246949 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32992975_1.fastq.gz	Fastqsanger.gz
	SRR32992975_2.fastq.gz	Fastqsanger.gz
	SRR32992976_1.fastq.gz	Fastqsanger.gz
	SRR32992976_2.fastq.gz	Fastqsanger.gz
	SRR32992977_1.fastq.gz	Fastqsanger.gz

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Glioblastoma quiescent cells hijack astrocyte-derived mitochondria to drive activation and malignancy

Project description:Glioblastoma quiescent cells hijack astrocyte-derived mitochondria to drive activation and malignancy

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Glioblastoma quiescent cells hijack astrocyte-derived mitochondria to drive activation and malignancy

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Project description:Quiescence is a reversible cell-cycle arrest used by Cancer Stem Cells (CSCs) to evade killing following conventional therapies. Quiescent CSCs are therefore one of the main cause of cancer recurrence. In glioblastoma, the most common and aggressive primary brain tumors, the quiescent glioblastoma stem-like cells (GSCs) are localized in hypoxic and acidic microenvironments and microenvironmental changes can control cell cycle re-entering of the GSCs. Here, we show that proliferating GSCs isolated from patients can be induced and maintained in a quiescent state by lowering the extracellular pH. Through RNA-seq analysis we characterized the RNA signatures of quiescent versus proliferating GSCs. We identified genes involved in the control of Ca2+ signaling and differentially expressed between the two states. Using the bioluminescent Ca2+ reporter EGFP-aequorin targeted to the mitochondria or the cytosol we explored the changes in Ca2+ homeostasis occurring during the switch from proliferation to quiescence. This remodeling is controlled through store-operated channels (SOCs). SOCs play a causal role since the inhibition of the Ca2+ influx through SOC drives proliferating GSCs to quiescence. We showed that the switch to quiescence is characterized by both an increased capacity of GSCs’ mitochondria to capture Ca2+ and a dramatic and reversible change of mitochondrial morphology from a tubular to a donut shape. Our data suggest that the remodeling of the Ca2+ homeostasis and the reshaping of mitochondria during the transition from proliferation to quiescence constitute a protective mechanism that favors cancer stem-like cells’ survival and their aggressiveness in glioblastoma.

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