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Synergism of FAK and ROS1 inhibitors in the treatment of CDH1-deficient cancers mediated by FAK-YAP-TRX signaling

ABSTRACT: Synergism of FAK and ROS1 inhibitors in the treatment of CDH1-deficient cancers mediated by FAK-YAP-TRX signaling

PROVIDER: PRJNA953390 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24106785_1.fastq.gz	Fastqsanger.gz
	SRR24106785_2.fastq.gz	Fastqsanger.gz
	SRR24106786_1.fastq.gz	Fastqsanger.gz
	SRR24106786_2.fastq.gz	Fastqsanger.gz
	SRR24106787_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Synergism of FAK and ROS1 inhibitors in the treatment of CDH1-deficient cancers mediated by FAK-YAP-TRX signaling

Project description:To investigate the ROS1 and FAK inhibitors combination may provide stronger anti-cancer effects by targeting CDH1 deficiency and potentially overcome drug resistance. Here, we evaluated the effects and mechanisms of combined treatment with FAK inhibitor IN10018 and ROS1 inhibitors.

2024-12-01 | GSE229195 | GEO

Synergism of FAK and ROS1 inhibitors in the treatment of <i>CDH1</i>-deficient cancers mediated by FAK-YAP signaling.

Project description:CDH1 deficiency is common in diffuse gastric cancer and triple negative breast cancer patients, both of which still lack effective therapeutics. ROS1 inhibition results in synthetic lethality in CDH1-deficient cancers, but often leads to adaptive resistance. Here, we demonstrate that upregulation of the FAK activity accompanies the emergence of resistance to ROS1 inhibitor therapy in gastric and breast CDH1-deficient cancers. FAK inhibition, either by FAK inhibitors or by knocking down its expression, resulted in higher cytotoxicity potency of the ROS1 inhibitor in CDH1-deficient cancer cell lines. Co-treatment of mice with the FAK inhibitor and ROS1 inhibitors also showed synergistic effects against CDH1-deficient cancers. Mechanistically, ROS1 inhibitors induce the FAK-YAP-TRX signaling, decreasing oxidative stress-related DNA damage and consequently reducing their anti-cancer effects. The FAK inhibitor suppresses the aberrant FAK-YAP-TRX signaling, reinforcing ROS1 inhibitor's cytotoxicity towards cancer cells. These findings support the use of FAK and ROS1 inhibitors as a combination therapeutic strategy in CDH1-deficient triple negative breast cancer and diffuse gastric cancer patients.

| S-EPMC10266074 | biostudies-literature

mRNA-seq of ros1-3 and ros1-4 with ABA treatment

Project description:To survey transcriptome changes by the mutations of a DNA demethylase ROS1 responding to a phytohormone abscisic acid, we performed the Next-gen sequencing (NGS) associated RNA-seq analysis. Two ROS1 knockout lines (ros1-3, ros1-4; Penterman et al. 2007 [PMID: 17409185]) with the wild-type Col line (wt) were subjected. Three samples (ros1-3, ros1-4 and wt), biological triplicates, ABA or mock treatment, using Illumina HiSeq 2500 system

2016-01-15 | E-GEOD-65016 | biostudies-arrayexpress

BS-seq of ros1-3, ros1-4 with wildtype col-0

Project description:To servey the methylome changes by mutation of a DNA demethylase ROS1, we performed the Next-gen sequencing (NGS) associated whole genome bisulfite sequencing (BS-seq) analysis. Two ROS1 knockout lines (ros1-3 and ros1-4; Penterman et al. 2007 [PMID: 17409185]) were subjected in this study.

2018-12-31 | GSE64569 | GEO

RNA sequencing of CDH1+/THY1+ and CDH1-/THY1+ germline stem cells

Project description:To futher understand the properties of CDH1+ GSCs and CDH1- GSCs, flow cytometry was used to sort the twopopulations after trypsin digestion and they were compared by total RNA sequencing (RNA-seq). The data clearlyshowed CDH1+ and CDH1- cells as having highly distinct profiles. In particular, numerous epithelial genes (e.g.Dsp, Pkp2, Krt19) were highly expressed in the CDH1+ population. In contrast, most genes known to be generalmarkers of SSCs/undifferentiated spermatogonia were downregulated (e.g. GFRA1 and ID4) or unchanged (e.g. ZBTB16and SALL4) in CDH1- GSCs. Additionally, KEGG pathway analysis revealed that the two populations exhibiteddistinctive activity in several signaling pathways including WNT and TGFb signaling. Notably, Tgfbr1, Smad2, Smad3tended to be lower in CDH1+ GSCs while Smad7, an inhibitor of TGFb signaling, was higher.The results showed thatCDH1+ GSCs were more epithelial in nature compared to CDH1- GSCs and supported the notion that CDH1+ GSCs are areable to partly overcome MET barrier because they may be in an advanced stage of MET.

2017-03-01 | GSE90712 | GEO

mRNA-seq of ros1-3 and ros1-4 with ABA treatment

2016-01-15 | GSE65016 | GEO

small RNA profiling of WT, ros1-4, nrpd1 single mutants and ros1-4/nrpd1doubble mutant [small RNA-seq]

Project description:Arabidopsis ROS1 is the first genetically characterized DNA demethylase in eukaryotes. Dysfunction of ROS1 leads to increase in DNA methylation level at thousands of genomic loci. However, the features of ROS1 targets are not well understood. In this study, we identified and characterized ROS1 target loci in Arabidopsis Col-0 and C24 ecotypes. Most ROS1 targets are transposable elements (TEs) and intergenic regions. Compared to other TEs, ROS1-targeted TEs are closer to protein coding genes, suggesting a role for ROS1 in preventing the spreading of DNA methylation from highly methylated TEs to nearby genes. Interestingly, we found that unlike general TEs, ROS1 targets are associated with an enrichment of H3K18ac and H3K27me3, and depletion of H3K27me and H3K9me2. We investigated the antagonism between ROS1 and RNA-directed DNA methylation (RdDM) by identifying and characterizing thousands of genomic regions regulated by both ROS1 and RdDM. Unexpectedly, we uncovered thousands of previously unidentified RdDM targets by analyzing the DNA methylome of ros1/nrpd1 double mutant plants. In addition, we show that ROS1 also antagonizes RdDM-independent DNA methylation at more than a thousand genomic loci. Our results provide significant insights into the genome-wide effects of both ROS1-mediated active DNA demethylation and RNA-directed DNA methylation as well as their interaction in plants. Using small RNA-Seq(sRNA-Seq) to get small RNA profiling of WT, ros1-4, nrpd1 single mutants and ros1-4/nrpd1doubble mutant

2016-11-01 | GSE83800 | GEO

plant-microbial synergism

Project description:plant-microbial synergism Metagenome

| PRJNA1039707 | ENA

MethlyC-Seq of ros1-13 mutant

Project description:Using MethylC-Seq to provide single-base resolution of DNA methylation status in ros1-13 mutant Whole genome methylation maps of ros1-13 (with 35S-SUC2 transgene) was generated using BS-seq

2015-02-05 | E-GEOD-58790 | biostudies-arrayexpress

TRX-1 Regulates SKN-1 Nuclear Localization Cell Non-Autonomously in Caenorhabditis elegans

Project description:The Caenorhabditis elegans oxidative stress response transcription factor, SKN-1, is essential for the maintenance of redox homeostasis and is a functional ortholog of the Nrf family of transcription factors. The numerous levels of regulation that govern these transcription factors underscore their importance. Here, we add a thioredoxin, encoded by trx-1, to the expansive list of SKN-1 regulators. We report that loss of trx-1 promotes nuclear localization of intestinal SKN-1 in a redox-independent, cell non-autonomous fashion from the ASJ neurons. Furthermore, this regulation is not general to the thioredoxin family, as two other C. elegans thioredoxins TRX-2 and TRX-3 do not play a role in this process. Moreover, TRX-1-dependent regulation requires signaling from the p38 MAPK signaling pathway. However, while TRX-1 regulates SKN-1 nuclear localization, SKN-1 transcriptional activity remains largely unaffected. Interestingly, RNA-Seq revealed that loss of trx-1 elicits a general, organism-wide down-regulation of several classes of genes; those encoding for collagens and lipid transport and localization being most prevalent. However, one prominent lipase-related gene, lips-6, is highly up regulated upon loss of trx-1 in a skn-1-dependent manner. Together, these results uncover a novel role for a thioredoxin in regulating intestinal SKN-1 nuclear localization in a cell non-autonomous manner, thereby contributing to the understanding of the processes involved in maintaining redox homeostasis throughout an organism.

2016-04-01 | GSE77976 | GEO

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