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Dexamethasone drives macrophage repolarization linked to increased triple-negative breast cancer aggressiveness

ABSTRACT: Dexamethasone drives macrophage repolarization linked to increased triple-negative breast cancer aggressiveness

PROVIDER: PRJNA1228551 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32492306_1.fastq.gz	Fastqsanger.gz
	SRR32492306_2.fastq.gz	Fastqsanger.gz
	SRR32492307_1.fastq.gz	Fastqsanger.gz
	SRR32492307_2.fastq.gz	Fastqsanger.gz
	SRR32492308_1.fastq.gz	Fastqsanger.gz

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Dexamethasone drives macrophage repolarization linked to increased triple-negative breast cancer aggressiveness

Project description:Glucocorticoids (GCs) are known for their anti-inflammatory potential, which includes macrophage polarization into an anti-inflammatory and tissue remodeling state. GCs are routinely co-administered to cancer patients to alleviate the side effects of chemotherapy. However, it is not well known if GCs can modulate tumor-associated macrophages (TAMs) to promote tumor progression. Here, we show that dexamethasone (DEX) induces dose-dependent differentiation of THP-1 monocyte-derived anti-tumorigenic (M1) macrophages into pro-tumorigenic (M2-like) macrophages, even in the presence of M1 cues, and that DEX can repolarize fully differentiated M1 macrophages into an M2-like state. These macrophages have a cytokine profile similar to the pro-tumorigenic (M2) macrophages and can stimulate the proliferation and invasion of triple-negative breast cancer (TNBC) cells in vitro. DEX treatment of an orthotopic mouse model of TNBC attenuated paclitaxel-mediated tumor growth inhibition, increased M2-like TAMs in primary tumors, and enhanced lung metastasis. Transcriptomic analysis of DEX-treated M1 macrophages revealed not only transcriptomic overlap to M2 macrophages, but to human breast cancer TAM transcriptomic data and further to a specific TAM signature associated with aggressive estrogen receptor-negative breast cancer. Our study illustrates a remarkable macrophage repolarization plasticity upon DEX exposure and warrants care in prescribing high doses of GCs to breast cancer patients, especially to those considered for chemotherapy.

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Rat liver: Dexamethasone treatment vs. Control

Project description:Sixteen male Sprague-Dawley rats were randomly allocated into 2 groups (8 rats per group) as follows: the control group (CON) and the dexamethasone-treated group (DEXA). Dexamethasone-treated rats received a daily intraperitoneal injection of 1.5 mg/kg of dexamethasone for 5 days. All rats were fasted during the night following the fifth day. On the sixth day, the animals were killed by decapitation. In order to focus our investigation on metabolism-related genes, we developed a metabolism dedicated microarray tool: the Mitoligo. Using this microarray tool, we were able to determine that energy metabolism was deeply modified by dexamethasone treatment. Dexamethasone treatment to rats induces a complete switch of the metabolism toward a maximal rate of ATP synthesis. In this study, we show that substrate supplying for oxidative phosphorylation is greatly enhanced. We also confirm that oxidative phosphorylation capacity is increased by dexamethasone treatment. Keywords: hormonal treatment

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Transcriptional and Functional Diversity of Macrophage Repolarization: Implications in Chronic Inflammation and Cystic Fibrosis

Project description:Macrophage plasticity allows cells to adopt different phenotypes, a property with potentially important implications in chronic pulmonary disorders such as cystic fibrosis (CF). We examined the transcriptional and functional significance of macrophage repolarization from an “M1” (LPS-stimulated) towards an “M2” phenotype using 5 stimuli. We found that macrophages exhibit highly diverse responses to distinct M2-polarizing stimuli. Specifically, we observed that IL-10 abrogated LPS-tolerance allowing for rapid restoration of LPS responsiveness. In contrast, IL-4 enhanced LPS-tolerance, dampening pro-inflammatory responses after repeat LPS challenge. We found enrichment of phagocytosis-associated pathways in macrophages stimulated with IL-10, leading them to display the greatest efferocytosis ability. Finally, we observed that CF macrophages had intact reparative responses, suggesting that macrophage contributions to CF lung disease are shaped by their environmental milieu and are modifiable. These findings highlight the diversity of macrophage activation states, attribute functional consequences to these stimuli, and provide a unique resource of human macrophage repolarization markers.

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Dexamethasone and lenalidomide have distinct functional effects on erythropoiesis

Project description:We explored the effects of dexamethasone and lenalidomide, individually and in combination, on the differentiation of primary human bone marrow progenitor cells in vitro. Both agents promote erythropoiesis, increasing the absolute number of erythroid cells produced from normal CD34+ cells and from CD34+ cells with the types of ribosome dysfunction found in DBA and del(5q) MDS. However, the drugs had distinct effects on the production of erythroid progenitor colonies; dexamethasone selectively increased the number burst-forming units-erythroid (BFU-E), while lenalidomide specifically increased colony-forming units-erythroid (CFU-E). Use of the drugs in combination demonstrates that their effects are not redundant.

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Effects of dexamethasone on gene expression in rat pancreatic AR42J cell line

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