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Quiescent ovarian cancer cells, in response to chemotherapy, secrete follistatin to induce chemotherapy resistance in surrounding cells.

ABSTRACT: Quiescent ovarian cancer cells, in response to chemotherapy, secrete follistatin to induce chemotherapy resistance in surrounding cells.

PROVIDER: PRJNA865730 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20791334_1.fastq.gz	Fastqsanger.gz
	SRR20791334_2.fastq.gz	Fastqsanger.gz
	SRR20791335_1.fastq.gz	Fastqsanger.gz
	SRR20791335_2.fastq.gz	Fastqsanger.gz
	SRR20791336_1.fastq.gz	Fastqsanger.gz

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Quiescent ovarian cancer cells, in response to chemotherapy, secrete follistatin to induce chemotherapy resistance in surrounding cells.

Project description:We sought to identify mechanism of NFATC4 quiescence-driven chemoresistance. RNA-Seq identified upregulation of follistatin (FST) in quiescent OvCa cells.

2022-08-10 | GSE210439 | GEO

Quiescent Ovarian Cancer Cells Secrete Follistatin to Induce Chemotherapy Resistance in Surrounding Cells in Response to Chemotherapy.

Project description:PurposeWe recently reported that the transcription factor NFATC4, in response to chemotherapy, drives cellular quiescence to increase ovarian cancer chemoresistance. The goal of this work was to better understand the mechanisms of NFATC4-driven ovarian cancer chemoresistance.Experimental designWe used RNA sequencing to identify NFATC4-mediated differential gene expression. CRISPR-Cas9 and FST (follistatin)-neutralizing antibodies were used to assess impact of loss of FST function on cell proliferation and chemoresistance. ELISA was used to quantify FST induction in patient samples and in vitro in response to chemotherapy.ResultsWe found that NFATC4 upregulates FST mRNA and protein expression predominantly in quiescent cells and FST is further upregulated following chemotherapy treatment. FST acts in at least a paracrine manner to induce a p-ATF2-dependent quiescent phenotype and chemoresistance in non-quiescent cells. Consistent with this, CRISPR knockout (KO) of FST in ovarian cancer cells or antibody-mediated neutralization of FST sensitizes ovarian cancer cells to chemotherapy treatment. Similarly, CRISPR KO of FST in tumors increased chemotherapy-mediated tumor eradication in an otherwise chemotherapy-resistant tumor model. Suggesting a role for FST in chemoresistance in patients, FST protein in the abdominal fluid of patients with ovarian cancer significantly increases within 24 hours of chemotherapy exposure. FST levels decline to baseline levels in patients no longer receiving chemotherapy with no evidence of disease. Furthermore, elevated FST expression in patient tumors is correlated with poor progression-free, post-progression-free, and overall survival.ConclusionsFST is a novel therapeutic target to improve ovarian cancer response to chemotherapy and potentially reduce recurrence rates.

| S-EPMC10192102 | biostudies-literature

Changes in follistatin levels by BRCA1 may serve as a regulator of ovarian carcinogenesis

Project description:Follistatin is a folliculogenesis regulating protein that has been found in relatively high concentration in the female ovarian tissues. Follistatin acts as an antagonist to the function of Activin, which is often found elevated in ovarian carcinogenesis and thus presents a possibility for therapeutic intervention in controlling ovarian cancer. Most of the ovarian cancer occurs in its ovarian surface epithelium (OSE) cells. Although breast cancer susceptibility gene 1 (BRCA1) is a known tumor suppressor for breast cancer but its role in ovarian cancer is beginning to unfold. We have shown that in ovarian carcinoma cells (SKOV3), stable overexpression of BRCA1 stimulates Follistatin secretion and simultaneously downregulates Activin expression. Moreover, knock down of BRCA1 in immortalized OSE (IOSE) cells from human ovarian tissue demonstrates downregulation of Follistatin secretion with simultaneous up regulation of Activin expression. IOSE cells generated from an ovarian cancer patient with BRCA1 mutation failed to secrete Follistatin in the medium. Our results indicate a novel function for BRCA1 in the form of regulation of the expression of Follistatin in the ovarian cells. 3 treatments vs 3 controls

2011-07-02 | E-GEOD-30296 | biostudies-arrayexpress

Changes in follistatin levels by BRCA1 may serve as a regulator of ovarian carcinogenesis

2011-07-02 | GSE30296 | GEO

Fasting-mimicking diet synergizes with ferroptosis against quiescent, chemotherapy-resistant cells

Project description:Fasting-mimicking diet synergizes with ferroptosis against quiescent, chemotherapy-resistant cells

| PRJNA885828 | ENA

Quiescent human glioblastoma cancer stem cells mediate tumor initiation, expansion, and recurrence following chemotherapy

Project description:Quiescent human glioblastoma cancer stem cells mediate tumor initiation, expansion, and recurrence following chemotherapy

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Endothelial cells exposed to atheroprotective flow secrete follistatin-like protein 1 which reduces transcytosis and inflammation

Project description:Objective - When endothelium is cultured in wells swirled on an orbital shaker, cells at the well centre experience putatively proatherogenic flow whereas those near the edge experience putatively atheroprotective flow. Transcellular transport is decreased equally in both regions, consistent with it being reduced by a mediator released from cells in one part of the well and mixed in the swirling medium. Here we identify the mediator and the flow characteristics that stimulate its release. Approach and Results - Medium conditioned by cells swirled at the edge, but not by cells swirled at the centre or cultured under static conditions, significantly reduced transendothelial transport of a low density lipoprotein (LDL)-sized tracer. Mass spectrometry identified follistatin-like 1 (FSTL1) as a candidate mediator. Cells from the swirled edge produced more FSTL1 than cells from the swirled centre or from static wells. Exogenous FSTL1 reduced transendothelial transport of the LDL-sized tracer and of LDL itself. An inhibitor of transcytosis similarly inhibited tracer transport. Exogenous FSTL1 and medium conditioned by cells swirled at the well edge also inhibited TNF-α-induced VCAM-1 and ICAM-1 expression, phosphorylation of IκBα, nuclear translocation of NF-κB, and monocyte adhesion. Conclusions - Putatively atheroprotective flow stimulates production of FSTL1 from cultured endothelial cells. FSTL1 reduces transcellular transport of LDL-sized particles and of LDL itself, and inhibits endothelial activation. If this also occurs in vivo, it may account for the atheroprotective nature of such flow. The identification of a mediator linking flow to LDL transport suggests novel therapeutic strategies.

2021-08-23 | PXD022068 | Pride

Quiescent and non-quiescent deletion-mutant strains

Project description:This SuperSeries is composed of the following subset Series: GSE8542: BY4742 Quiescent and Non-quiescent replicates GSE8558: Proteinase K treatment of Q and NQ cells GSE8559: S288c Quiescent and Non-quiescent replicates GSE8560: Mutant1 GSE8561: Mutant2 Refer to individual Series

2010-05-29 | E-GEOD-8624 | biostudies-arrayexpress

HMEC Quiescent single cells

Project description:Gene expression after mammosphere culture, quiescent single cells

| EGAD00010001964 | EGA

Kmt2c-mutations superimpose properties of activated and quiescent HSCs to convey a selective advantage after chemotherapy

Project description:Kmt2c-mutations superimpose properties of activated and quiescent HSCs to convey a selective advantage after chemotherapy

| PRJNA664131 | ENA