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MCPIP1 controls effects of myeloid cells on skin carcinogenesis and hair growth

ABSTRACT: MCPIP1 controls effects of myeloid cells on skin carcinogenesis and hair growth

PROVIDER: PRJNA1011806 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25867532.fastq.gz	Fastqsanger.gz
	SRR25867533.fastq.gz	Fastqsanger.gz
	SRR25867534.fastq.gz	Fastqsanger.gz
	SRR25867535.fastq.gz	Fastqsanger.gz
	SRR25867536.fastq.gz	Fastqsanger.gz

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MCPIP1 controls effects of myeloid cells on skin carcinogenesis and hair growth

Project description:Depletion of Mcpip1 in the cells of myeloid origin modifies the sensitivity to the cutaneous chemical carcinogenesis. It attenuates epidermal proliferation and increases the susceptibility to the formation of melanocytic nevi. Thus, myeloid Mcpip1 is an important modulator in the course of skin carcinogenesis.

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Distinct roles of keratinocyte- and myeloid- MCPIP1 in maintaining skin homeostasis

Project description:The morphology of the skin changes upon depletion of MCPIP1 in cells of myeloid origin as well as in keratinocytes. The thicknesses of epidermal and hypodermal layers are significantly increased in mice with loss of epidermal MCPIP1, whereas loss of myeloid MCPIP1 exerts completely opposite effect. Both types of mice show contrary response to the stimulation with 12-O-tetradecanoylphorbol-13-acetate. Skin morphology and inflammatory phenotype of keratinocyte- and myeloid- double MCPIP1 knockout mice is similar to that of the single keratinocyte knockout of MCPIP1. In all, myeloid and epidermal MCPIP1 play significant but distinct roles in the modulation of skin-related processes. This study was funded by National Science Centre grant numbers 2020/37/N/NZ5/00575 (to Weronika Szukala) and 2021/41/B/NZ5/03601 (to Jolanta Jura)."

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Distinct roles of keratinocyte- and myeloid- MCPIP1 in maintaining skin homeostasis

Project description:Distinct roles of keratinocyte- and myeloid- MCPIP1 in maintaining skin homeostasis

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Regulation of miRNA biogenesis by MCPIP1

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MCPIP1 functions as a safeguard of early embryonic development

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Integrative genomics reveal a role for MCPIP1 in adipogenesis and adipocyte metabolism

Project description:Obesity is considered a serious chronic disease, which is associated with increased risk of developing cardiovascular diseases, non-alcoholic fatty liver disease and type 2 diabetes. Monocyte chemoattractant protein-1-induced protein-1 (MCPIP1), also called Regnase-1, is an RNase that decreases stability of transcripts coding for inflammation-related proteins. In addition, MCPIP1 plays an important role in the regulation of adipogenesis in vitro by reducing the expression of key transcription factors, including C/EBPβ and PPARγ, during adipocyte differentiation. Here we present RNA-Seq and proteomic analysis of 3T3-L1 adipocytes overexpressing wild-type MCPIP1 (WTMCPIP1) and mutant MCPIP1 (D141NMCPIP1) at day 2 and 4 of differentiation, respectively. RNA-Seq analysis followed by confirmatory Q-RT-PCR revealed that elevated MCPIP1 levels in 3T3-L1 adipocytes upregulated transcripts encoding proteins involved in signal transmission and cellular remodeling and downregulated transcripts of factors involved in metabolism. These data are consistent with our LC-MS/MS analysis, which showed that MCPIP1 expressing adipocytes exhibit upregulation of proteins involved in cellular organization and movement and decreased levels of proteins involved in lipid and carbohydrate metabolism. Moreover, MCPIP1 adipocytes are characterized by decreased Glut4 levels and impaired glucose uptake. Overall, our ﬁndings demonstrate that MCPIP1 is an important regulator of adipogenesis and adipocyte metabolism.

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Small RNAseq of MV3 melanoma cells overexpressing MCPIP1 protein

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Project description:Epigenetic regulation is a pivotal factor during neuroblastoma (NB) pathogenesis and investigations into cancer epigenetics are actively underway to identify novel therapeutic strategies for NB patients. SUV39H1, a member of the H3K9 methyltransferase family, contributing to tumorigenesis across multiple malignancies. However, its specific role in NB remains unexplored. In this study, we conducted a high-throughput screen utilizing a compound library containing 288 epigenetic drugs, leading to the identification of chaetocin as the most potent NB inhibitor by targeting SUV39H1. Genetic manipulation and therapeutic inhibition of SUV39H1 significantly impacted proliferation, migration, cell cycle phases, and apoptosis in NB cells. Concurrently, chaetocin demonstrated robust anti-tumor efficacy in vivo with tolerable toxicity. RNA-seq unveiled that SUV39H1 knockdown and inhibition down-regulated cell cycle pathways, impacting vital genes such as AURKA. Besides, MCPIP1 emerged as a novel tumor suppressor following SUV39H1 inhibition, which decreased AURKA expression in NB. In detail, SUV39H1 mediated the enrichment of H3K9me3 at the promoter region of MCPIP1, repressing the MCPIP1-mediated degradation of AURKA and facilitating the subsequent accumulation of AURKA, which revealed the oncogenic role of SUV39H1 via the SUV39H1-MCPIP1-AURKA signaling axis in NB. Therapeutic inhibition of SUV39H1 using chaetocin emerges as an effective and safe strategy for NB patients.

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