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Estrogen receptor and mTOR signaling rewires cancer metabolism in obesity-associated breast cancer

ABSTRACT: Estrogen receptor and mTOR signaling rewires cancer metabolism in obesity-associated breast cancer

PROVIDER: PRJNA471101 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7156190.fastq.gz	Fastqsanger.gz
	SRR7156185.fastq.gz	Fastqsanger.gz
	SRR7156186.fastq.gz	Fastqsanger.gz
	SRR7156187.fastq.gz	Fastqsanger.gz
	SRR7156188.fastq.gz	Fastqsanger.gz

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Estrogen receptor and mTOR signaling rewires cancer metabolism in obesity-associated breast cancer

Project description:Obesity is a risk factor for postmenopausal ERα (+) breast cancer. Molecular mechanisms activated by the factors from serum that contribute to this risk and how these mechanisms affect ERα signaling are yet to be elucidated. To identify such mechanisms, we performed whole metabolite and protein profiling in serum samples, which enabled us to focus on factors that were differentially present in serum from cancer-free vs. breast cancer susceptible and obese vs. non-obese post-menopausal women. These studies combined with in vitro assays identified free fatty acids (FFAs), as serum factors that correlate with increased proliferation and aggressiveness in ERα(+) breast cancer cells by. FFAs activated both ERα and mTOR pathways and rewired metabolism in breast cancer cells. Pathway preferential estrogen-1 (PaPE-1), which target ERα and mTOR signaling, was able to block changes induced by FFAs. In fact, PaPEs were more effective in the presence of FFAs, suggesting a role for obesity-associated gene and metabolic rewiring in providing new targetable vulnerabilities for ERα-(+) breast cancer in postmenopausal women. Our findings provide a basis for preventing or inhibiting obesity-associated breast cancer by using PaPEs that would reverse these newly appreciated metabolic properties of breast tumors in obese postmenopausal women.

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Estrogen Receptor α (ERα)-mTOR signaling crosstalk rewires cancer cell metabolism providing a mechanism underlying obesity-associated postmenopausal breast cancer

Project description:Estrogen Receptor α (ERα)-mTOR signaling crosstalk rewires cancer cell metabolism providing a mechanism underlying obesity-associated postmenopausal breast cancer

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Estrogen Receptor α (ERα)-mTOR signaling crosstalk rewires cancer cell metabolism providing a mechanism underlying obesity-associated postmenopausal breast cancer [ChIP-seq]

Project description:Obesity is a risk factor for postmenopausal ERα (+) breast cancer. The metabolites from serum that contribute to this risk and how these factors affect ERα signaling are not known. Using whole metabolite profiling and a detection panel for proteins, we identified biomarkers that were differentially present in serum from obese vs. non-obese postmenopausal women, and we validated these factors in two separate cohorts of postmenopausal women who either developed breast cancer or those who were obese and lost weight after the onset of menopause. In vitro assays identified free fatty acids (FFAs), in particular oleic acid (OA) as serum factors that correlate with increased proliferation and aggressiveness in ERα(+) breast cancer cells by. FFAs activated both ERα and mTOR pathways and rewired metabolism in breast cancer cells. Pathway preferential estrogen-1 (PaPE-1), which target ERα and mTOR signaling, was able to block changes induced by FFAs. In fact, PaPEs were more effective in the presence of FFAs, suggesting a role for obesity-associated gene and metabolic rewiring in providing new targetable vulnerabilities for ERα-(+) breast cancer in postmenopausal women. Our findings provide a basis for preventing or inhibiting obesity-associated breast cancer by using PaPEs that would reverse these newly appreciated metabolic vulnerabilities of breast tumors in obese postmenopausal women.

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Estrogen Receptor α (ERα)-mTOR signaling crosstalk rewires cancer cell metabolism providing a mechanism underlying obesity-associated postmenopausal breast cancer [RNA-seq]

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Estrogen sensing by GPER1 activates PI3K/mTOR to promote gender dimorphism in liver growth and cancer

Project description:Liver cancer is a common cause of cancer death, with a male-predominant incidence due, in part, to increased estrogen levels in cirrhotic patients. It is unknown, however, how estrogen is sensed to influence this process. Here, we show that estrogen activates the G protein-coupled estrogen receptor 1 (GPER1), expressed in hepatocytes, to enhancing hepatocyte size, cell cycle progression and cell proliferation, thereby increasing liver growth in zebrafish larvae and adults. GPER1 stimulation activates PI3K/mTOR signaling, and mTOR is essential for both normal and regenerative organ growth. Genetic loss of GPER1 diminishes and estrogen exposure accelerates chemical carcinogenesis, specifically in males. Chemical inhibition of GPER1 significantly reduces cancer incidence and progression in a gender-specific fashion. Our studies identify GPER1 as a hepatic estrogen sensor that mediates gender dimorphic growth, mTOR activation, and can serve as a therapeutic target for liver cancer treatment.

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Project description:Epidemiological studies highlight a strong association between obesity and colorectal cancer (CRC). This association appears stronger in men and a role for sex hormones is indicated by epidemiological studies. Especially estrogen is protective against CRC and correlated to several aspects of the metabolic syndrome. Anti-inflammatory and anti-tumorigenic effects of estrogen in colon have been demonstrated to act via estrogen receptor beta (ERβ). This led us to hypothesize that estrogenic signaling, through both systemic and local effects might modulate the colon microenvironment during HFD-induced obesity. In order to test our hypothesis mice were fed a control diet or a high fat diet (HFD) for 3 weeks and treated with different estrogenic ligands. In the present study, we demonstrate that there are sex-differences in the response to HFD-induced obesity and in the colon transcriptome. Both sexes develop obesity with an impaired circadian rhythm but the male metabolic profile is more sensitive to HFD and increased the colon epithelial cell proliferation. Females were resistant to impaired glucose metabolism, but HFD-feeding increased the infiltration of macrophages. Estrogen signaling in males, via ERα, presented anti-obesogenic effects. However, systemic and/or local activation of both ERα and ERβ restored the circadian rhythm in the males. In females, systemic activation of ERα restored the circadian rhythm, however, systemic and/or local activation of ERβ down-regulated the expression of macrophage markers. These results suggest that estrogen signaling through systemic and/or local activation of ERβ can regulate the colon microenvironment during HFD-induced obesity.

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FGF1 supports metabolic reprogramming through the estrogen receptor in endocrine-resistant and obesity-associated breast cancer

Project description:Obesity is associated with elevated breast cancer risk and with breast cancer-specific mortality, particularly for people with estrogen receptor (ER) positive tumors. Body mass index (BMI) is commonly used to define obesity, but it may not be the best predictor of breast cancer risk or prognosis on an individual level. Adult weight gain is an independent prognostic indicator of breast cancer risk, and many patients undergoing cancer treatment experience the side effect of weight gain. Our previous work described a murine model of obesity, ER-positive breast cancer, and weight gain, and identified fibroblast growth factor receptor (FGFR) as a potential driver of tumor progression in some cases. During adipose tissue expansion, the FGF1 ligand is produced by hypertrophic adipocytes as a stimulus to stromal preadipocytes that proliferate and differentiate to provide additional lipid storage capacity. In the breast adipose tissue, FGF1 production may stimulate cancer cell proliferation and tumor progression.

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