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Tumor-derived oxidative stress triggers follicle loss in breast cancer

ABSTRACT: Tumor-derived oxidative stress triggers follicle loss in breast cancer

PROVIDER: PRJNA858670 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20187151.fastq.gz	Fastqsanger.gz
	SRR20187152.fastq.gz	Fastqsanger.gz
	SRR20187153.fastq.gz	Fastqsanger.gz
	SRR20187154.fastq.gz	Fastqsanger.gz
	SRR20187155.fastq.gz	Fastqsanger.gz

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Tumor-derived oxidative stress triggers follicle loss in breast cancer

Project description:Breast cancer is the common indication for ovarian cryopreservation. However, whether the grafting ovarian tissue meets the functional requirements and the need for additional interventions remains unclear. Here, we show abnormal serum hormones in breast cancer in human and tumor-bearing mice, and for the first time show that tumor induced loss of primordial and growing follicles and the number of follicles being lost to either growth or atresia. A gene signature of tumor-bearing mice demonstrates the disturbed regulatory network of steroidgenesis which link to mitochnondia dysfunction in oocytes and granulosa cells via PI3K signaling pathway.

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Priming mobilization of hair follicle stem cells triggers permanent loss of regeneration after alkylating chemotherapy

Project description:The maintenance of genetic integrity is critical for stem cells to ensure homeostasis and regeneration. Little is known about how adult stem cells respond to irreversible DNA damage, resulting in loss of regeneration in humans. Here, we establish a permanent regeneration loss model using cycling human hair follicles treated with alkylating agents: busulfan followed by cyclophosphamide. We unravel the underlying mechanisms by which hair follicle stem cells (HFSCs) lose their pool. Contrary to immediate destructive changes in rapidly proliferating hair matrix cells, quiescent HFSCs show unexpected massive proliferation after busulfan and then undergo large-scale apoptosis following cyclophosphamide. HFSC proliferation is activated through PI3K/Akt pathway, and depletion is driven by p53/p38-induced cell death. RNA-seq analysis shows that HFSCs experience mitotic catastrophe with G2/M checkpoint activation. Our findings indicate that priming mobilization causes stem cells to lose their resistance to DNA damage, resulting in permanent loss of regeneration after alkylating chemotherapy.

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Bisphenol A triggers apoptosis in mouse pre-antral follicle granulosa cells via oxidative stress.

Project description:BackgroundBisphenol A (BPA), an endocrine disrupting chemical with weak estrogenic and anti-androgenic activity, is widely present in various environmental media and organisms. It has certain reproductive toxicity and can cause a variety of female reproductive system diseases. Although BPA-stimulated apoptosis of granulosa cells has been widely elaborated, the effect of BPA on mouse pre-antral follicle granulosa cells (mpGCs) has not been well elucidated.ResultsIn this study, the results of live-dead cell staining showed that high concentrations of BPA severely impaired mpGCs growth viability and affected the cell cycle transition of mpGCs. We confirmed that BPA promotes the production of reactive oxygen species (ROS) and facilitates oxidative stress in mpGCs. In addition, immunofluorescence, transmission electron microscopy, and flow cytometry experiments demonstrated that BPA treatment for mpGCs resulted in apoptotic features, such as rounding, cytoplasmic crinkling, and mitochondrial damage. This was accompanied by a large production of ROS and apoptosis-inducing factor (AIF) translocation from the mitochondria to the nucleus. RNA-seq data showed that several apoptosis-related pathways were enriched in the high concentration BPA-treated group compared with the normal group, such as the p53 pathway, MAPK pathway, etc. CONCLUSIONS: These results suggest that cells undergo oxidative stress effects and apoptosis after BPA treatment for mpGCs, which affects normal follicle development. The potential mechanism of BPA-induced female reproductive toxicity was elucidated, while providing a research basis for the prevention and treatment of female reproductive diseases.

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Intermittent fasting triggers interorgan communication to suppress hair follicle regeneration

Project description:Intermittent fasting has gained increasing popularity globally for its potential benefits for improving health and managing weight, but how it impacts the homeostasis and regeneration of peripheral tissues remains elusive. Here we report that in mice, commonly used intermittent fasting regimens negatively affect hair regeneration by selectively inducing apoptosis in activated hair follicle stem cells (HFSCs). Through manipulating animals' daily feeding schedules and caloric intake, we have found that the impaired hair regeneration is primarily caused by the extended fasting periods within these regimens, rather than a reduction in total caloric intake or alterations in circadian rhythm. As the fasting period lengthens, the severity of the defects worsens. Mechanistically, extended periods of fasting activate the hypothalamic-pituitary-adrenal axis, prompting the release of lipolytic hormones from the adrenal glands into circulation. This triggers rapid lipolysis in dermal adipocytes, elevating levels of free fatty acids within the skin. Consequently, fatty acid oxidation is activated in HFSCs, causing increased cellular oxidative stress and apoptosis. Surgical removal of adrenal glands, genetic inhibition of fatty acid oxidation in HFSCs, or enhancement of HFSCs’ antioxidant capability genetically or pharmaceutically prevents fasting-induced stem cell death. Our study reveals a detrimental effect of intermittent fasting on somatic stem cells and peripheral tissue regeneration, and identifies a close crosstalk between an ancient neuroendocrine mechanism and a critical niche component that functions as a “brake” to halt tissue regeneration when the supply of nutrients becomes unstable.

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