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CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer [RNA-seq]

ABSTRACT: CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer [RNA-seq]

PROVIDER: PRJNA660171 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12545962.fastq.gz	Fastqsanger.gz
	SRR12545963.fastq.gz	Fastqsanger.gz
	SRR12545964.fastq.gz	Fastqsanger.gz
	SRR12545965.fastq.gz	Fastqsanger.gz
	SRR12545966.fastq.gz	Fastqsanger.gz

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Similar Datasets

CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer [CUT&RUN]

Project description:Cancer cells exploit adaptive responses such as endoplasmic reticulum (ER) stress to support their survival. ER stress response is mediated in part by the ER-localized transmembrane sensor IRE1α endoribonuclease and its substrate XBP1 to regulate XBP1 target gene expression. However, the mechanism that controls the IRE1α/XBP1 pathway remains poorly understood. CARM1 is an oncogene that is often overexpressed in a number of cancer types including ovarian cancer. Here we report that CARM1 determines ER stress response by controlling the IRE1α/XBP1 pathway. Genome-wide profiling revealed that CARM1 regulates XBP1 target gene expression during ER stress response. CARM1 directly interacts with XBP1. Inhibition of the IRE1α/XBP1 pathway was effective in ovarian cancer in a CARM1-dependent manner both in vitro and in vivo in orthotopic and patient-derived xenograft models. In addition, IRE1α inhibitor B-I09 synergizes with immune checkpoint blockade anti-PD1 antibody in an immunocompetent CARM1-expressing ovarian cancer model.

2021-08-11 | GSE157117 | GEO

CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer [RNA-seq]

2021-08-11 | GSE157116 | GEO

CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer

Project description:CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer

| PRJNA660169 | ENA

CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer [CUT&RUN]

Project description:CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer [CUT&RUN]

| PRJNA660172 | ENA

CARM1 determines endoplasmic reticulum stress response by controlling XBP1 in ovarian cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-08-11 | GSE157118 | GEO

Analysis of the IRE1/XBP1 unfolded protein response (UPR) pathway in Schmid metaphyseal chondrodysplasia hypertrophic chondrocyte endoplasmic reticulum (ER) stress

Project description:We set out to determine the role of the IRE1/XBP1 pathway, the most ancient and highly conserved endoplasmic reticulum (ER) stress-sensing pathway of the unfolded protein response (UPR), in Schmid metaphyseal chondrodysplasia (MCDS). RNA derived from hypertrophic zones microdissected from growth plates of wildtype mice, mice lacking XBP1 activity in chondrocytes (Xbp1Cart?Ex2), mice carrying a COL10A1 pN617K mutation (ColXN617K), and compound mutants (C/X) was analyzed by whole genome microarray analysis. 1633 probes were differentially expressed between ColXN617K and wildtype, 215 probes were differentially expressed between Xbp1Cart?Ex2 and wildtype, and 1337 probes were differentially expressed between C/X and wildtype. 885 probes were differentially expressed between ColXN617K and wildtype but not Xbp1Cart?Ex2 and wildtype or C/X and wildtype, thus representing the XBP1-dependent response to hypertrophic chondrocyte ER stress. 688 probes were differentially expressed between ColXN617K and wildtype and between C/X and wildtype but not Xbp1Cart?Ex2 and wildtype, thus representing the XBP1-independent response to hypertrophic chondrocyte ER stress. Results were validated by qPCR. Entire growth plate hypertrophic zones were microdissected from one tibia from each of three 2-week old wildtype mice, three 2-week old mice carrying a COL10A1 p.N617K mutation (ColXN617K), three 2-week old mice lacking XBP1 activity in chondrocytes (Xbp1Cart?Ex2), and three 2-week old mice resulting from a cross between ColXN617K and Xbp1Cart?Ex2 (C/X).

2015-08-21 | E-GEOD-72261 | biostudies-arrayexpress

Targeting the IRE1α/XBP1 endoplasmic reticulum stress response pathway in ARID1Amutant ovarian cancers

Project description:Targeting the IRE1α/XBP1 endoplasmic reticulum stress response pathway in ARID1Amutant ovarian cancers

| PRJNA748370 | ENA

Analysis of the IRE1/XBP1 unfolded protein response (UPR) pathway in Schmid metaphyseal chondrodysplasia hypertrophic chondrocyte endoplasmic reticulum (ER) stress

Project description:We set out to determine the role of the IRE1/XBP1 pathway, the most ancient and highly conserved endoplasmic reticulum (ER) stress-sensing pathway of the unfolded protein response (UPR), in Schmid metaphyseal chondrodysplasia (MCDS). RNA derived from hypertrophic zones microdissected from growth plates of wildtype mice, mice lacking XBP1 activity in chondrocytes (Xbp1CartΔEx2), mice carrying a COL10A1 pN617K mutation (ColXN617K), and compound mutants (C/X) was analyzed by whole genome microarray analysis. 1633 probes were differentially expressed between ColXN617K and wildtype, 215 probes were differentially expressed between Xbp1CartΔEx2 and wildtype, and 1337 probes were differentially expressed between C/X and wildtype. 885 probes were differentially expressed between ColXN617K and wildtype but not Xbp1CartΔEx2 and wildtype or C/X and wildtype, thus representing the XBP1-dependent response to hypertrophic chondrocyte ER stress. 688 probes were differentially expressed between ColXN617K and wildtype and between C/X and wildtype but not Xbp1CartΔEx2 and wildtype, thus representing the XBP1-independent response to hypertrophic chondrocyte ER stress. Results were validated by qPCR.

2015-08-21 | GSE72261 | GEO

Extracellular vesicles from human umbilical cord mesenchymal stem cells protect grafted islets against endoplasmic reticulum stress-induced mitochondrial dysfunction by modulating XBP1-based calcium homeostasis

Project description:Islet transplantation is an ideal option for diabetes while early graft lose serves as a major obstacle. Human umbilical cord mesenchymal stem cells (hucMSC) have multiple functions including the maintenance of cellular homeostasis. However, it is unknown whether extracellular vesicles (EVs) derived from hucMSC (hucMSC-EVs) provide protective effects against transplant-related trauma-induced islet injury. Here, we isolated and purified hucMSC-EVs, and found that hucMSC-EVs promoted grafted islet survival, and enhanced glycemic control following co-transplantation in a syngeneic streptozotocin (STZ)-induced mouse model of diabetes. After co-cultured for 12 h or 24 h, labelled hucMSC-EVs with PKH67 were readily internalized by NIT-1 β cells and islets. In tunicamycin (Tm) and thapsigargin (Tg) induced specific endoplasmic reticulum stress (ERS) cell injury models, hucMSC-EVs treatment improved cell viability and β cells function both in NIT-1 cells and ex vivo primary islets. Bulk RNA-seq demonstrated that hucMSC-EVs treatment significantly involved in ERS and the negative regulated mitochondrial apoptotic pathway. While ERS promoted interactions between endoplasmic reticulum (ER) and mitochondria, hucMSC-EVs alleviated ERS, maintained calcium homeostasis, and improved mitochondrial energy metabolism. Notably, the downregulation of XBP1 by hucMSC-EVs fine-tuned ER-mitochondria communication via reducing inositol-1,4,5-trisphosphate receptors at mitochondria-associated membranes (MAMs). Reduced XBP1 also activated Nrf2, restoring mitochondrial calcium homeostasis under ERS. miRNA analysis identified miR-182-5p enriched in hucMSC-EVs that specifically targeted XBP1 mRNA, leading to its degradation and downregulation. These findings demonstrate that hucMSC-EVs protect grafted islets by blocking XBP1 and restoring calcium homeostasis, thus suggesting their potential as a cell-free therapy for improving islet transplantation outcomes.

2025-11-02 | GSE296373 | GEO

Epithelial endoplasmic reticulum stress orchestrates a protective IgA response II

Project description:Immunoglobulin A (IgA) is the major secretory immunoglobulin isotype at mucosal surfaces where it regulates microbial commensalism and excludes luminal factors from contacting intestinal epithelial cells (IEC). IEC endoplasmic reticulum (ER) stress induces a polyreactive IgA response which protects from small intestinal inflammation. IEC ER stress causes expansion and activation of peritoneal B1b cells independent of microbiota and T cells that culminates in increased lamina propria and luminal IgA. Xbp1dIEC mice exhibit IEC ER stress by conditional deletion of X-box-binding protein 1 (XBP1). Here we examine single-cell transcriptomes of peritoneal cavity cells of germ-free Xbp1dIEC mice (KO) compared to littermate controls (WT).

2019-02-28 | GSE124562 | GEO

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