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Progressive Senescence Programs Elicit Intrinsic Vulnerability to Ageing-related Cancer

ABSTRACT: Progressive Senescence Programs Elicit Intrinsic Vulnerability to Ageing-related Cancer

PROVIDER: PRJNA801627 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17805900_1.fastq.gz	Fastqsanger.gz
	SRR17805900_2.fastq.gz	Fastqsanger.gz
	SRR17805901_1.fastq.gz	Fastqsanger.gz
	SRR17805901_2.fastq.gz	Fastqsanger.gz
	SRR17805902_1.fastq.gz	Fastqsanger.gz

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Progressive Senescence Programs Elicit Intrinsic Vulnerability to Ageing-related Cancer

Project description:Cancer incidence escalates exponentially with advancing age, the mechanism of which remains obscure. Here we built up a chronological molecular clock at the single cell level for the mammary stem cell enriched population to depict the physiological ageing dynamics. We found the mammary ageing process was asynchronous and progressive, determined by the relative proportions of four distinct cellular states. The mammary ageing was initiated by a light senescence state with elevated NFkb, P53 signals, followed by a deep senescence state with reduced NFkb, P53 and enhanced PI3K-Akt-mTOR, Wnt, Notch and pluripotency activities succumb to cancer predisposition. Both of these senescence programs were regulated by a master mammary stem cell factor Bcl11b through modulation of multiple stress, longevity and pluripotency associated pathways. Depletion of Bcl11b triggered morphological, functional and molecular ageing-like phenotypes, and drastically enhanced DMBA-induced tumor formation. We further screened out a drug TPCA-1 that can elevate Bcl11b activity, rejuvenate mammary cells transcriptomically and significantly reduce the ageing-related cancer incidence. Our findings established a molecular portrait of progressive mammary cell ageing and elucidated the regulatory network bridging mammary ageing and cancer predisposition that can be modulated to control the cancer initiation, which has potential implications in management of cancer prevalence.

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Increased intron retention is a post-transcriptional signature associated with progressive ageing and Alzheimer’s disease

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Project description:Cancer incidence escalates exponentially with advancing age; however, the underlying mechanism remains unclear. In this study, we build a chronological molecular clock at single-cell transcription level with a mammary stem cell-enriched population to depict physiological aging dynamics in female mice. We find that the mammary aging process is asynchronous and progressive, initiated by an early senescence program, succeeded by an entropic late senescence program with elevated cancer associated pathways, vulnerable to cancer predisposition. The transition towards senescence program is governed by a stem cell factor Bcl11b, loss of which accelerates mammary ageing with enhanced DMBA-induced tumor formation. We have identified a drug TPCA-1 that can rejuvenate mammary cells and significantly reduce aging-related cancer incidence. Our findings establish a molecular portrait of progressive mammary cell aging and elucidate the transcriptional regulatory network bridging mammary aging and cancer predisposition, which has potential implications for the management of cancer prevalence in the aged.

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