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Targeting Dual-specificity Phosphatase 23 to Overcome Chemoresistance and Stem Cell-like Behavior in Non-small Cell Lung Cancer Cells

ABSTRACT: Targeting Dual-specificity Phosphatase 23 to Overcome Chemoresistance and Stem Cell-like Behavior in Non-small Cell Lung Cancer Cells

PROVIDER: PRJNA1215748 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32127680_1.fastq.gz	Fastqsanger.gz
	SRR32127680_2.fastq.gz	Fastqsanger.gz
	SRR32127681_1.fastq.gz	Fastqsanger.gz
	SRR32127681_2.fastq.gz	Fastqsanger.gz
	SRR32127682_1.fastq.gz	Fastqsanger.gz

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Targeting Dual-specificity Phosphatase 23 to Overcome Chemoresistance and Stem Cell-like Behavior in Non-small Cell Lung Cancer Cells

Project description:Chemoresistance poses a significant challenge in treating non-small cell lung cancer (NSCLC), often leading to poor outcomes. This resistance is closely linked to cancer stem cell (CSC)-like characteristics, including the ability to evade anoikis. In this study, we identified dual-specificity phosphatase 23 (DUSP23) as a key molecule involved in regulating CSC traits and chemoresistance. DUSP23 expression was significantly elevated in cell clusters grown under ultra-low adhesion (ULA) conditions that mimic CSC-promoting environments. Silencing DUSP23 reduced the formation of these clusters, suppressed the expression of the stemness markers SOX2, and enhanced anoikis sensitivity. Additionally, in cisplatin-resistant NSCLC cells, knockdown of DUSP23 decreased invasive behavior and induced apoptosis. These findings suggest that DUSP23 plays a pivotal role in maintaining CSC-like properties and chemoresistance by regulating SOX2. Targeting DUSP23 could offer a novel approach to overcome treatment resistance and improve outcomes for patients with NSCLC.

2025-01-31 | GSE288032 | GEO

Induction of a timed metabolic collapse to overcome cancer chemoresistance

Project description:Induction of a timed metabolic collapse to overcome cancer chemoresistance

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Targeting cell cycle and apoptosis to overcome chemoresistance in AML

Project description:Targeting cell cycle and apoptosis to overcome chemoresistance in AML

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Dual-specificity phosphatase 23 mediates GCM1 dephosphorylation and activation.

Project description:Glial cells missing homolog 1 (GCM1) is a transcription factor essential for placental development. GCM1 promotes syncytiotrophoblast formation and placental vasculogenesis by activating fusogenic and proangiogenic gene expression in placenta. GCM1 activity is regulated by multiple post-translational modifications. The cAMP/PKA-signaling pathway promotes CBP-mediated GCM1 acetylation and stabilizes GCM1, whereas hypoxia-induced GSK-3β-mediated phosphorylation of Ser322 causes GCM1 ubiquitination and degradation. How and whether complex modifications of GCM1 are coordinated is not known. Here we show that the interaction of GCM1 and dual-specificity phosphatase 23 (DUSP23) is enhanced by PKA-dependent phosphorylation of GCM1 on Ser269 and Ser275. The recruitment of DUSP23 reverses GSK-3β-mediated Ser322 phosphorylation, which in turn promotes GCM1 acetylation, stabilization and activation. Supporting a central role in coordinating GCM1 modifications, knockdown of DUSP23 suppressed GCM1 target gene expression and placental cell fusion. Our study identifies DUSP23 as a novel factor that promotes placental cell fusion and reveals a complex regulation of GCM1 activity by coordinated phosphorylation, dephosphorylation and acetylation.

| S-EPMC3035457 | biostudies-literature

Homo sapiens

Project description:Targeting Dual-specificity Phosphatase 23 to Overcome Chemoresistance and Stem Cell-like Behavior in Non-small Cell Lung Cancer Cells

| PRJNA1215600 | ENA

Global Stability Profling of Colorectal Cancer Chemoresistance

Project description:Almost half of the patients with advanced colorectal cancer (CRC) are resistant to oxaliplatin based therapy, the first line treatment for CRC. Therefore, predicting and understanding oxaliplatin resistance is important to improve CRC patient survival. Investigated here is the use of proteomic folding stability measurements to differentiate oxaliplatin resistant and sensitive CRCs using patient-derived CRC cell lines and patient-derived xenografts (PDXs). Three protein stability profiling techniques (including the Stability of Proteins from Rates of Oxidation (SPROX), the Thermal Protein Profiling (TPP), and Limited Proteolysis (LiP) approaches) were employed to identify differentially stabilized proteins in 6 patient-derived CRC cell lines with different oxaliplatin sensitivities and 8 CRC PDXs derived from 2 of the patient derived cell lines with different oxaliplatin sensitivity. A total of 23 proteins were found in at least 2 techniques to be differentially stabilized in both the cell line and PDX studies of oxaliplatin resistance. These 23 differentially stabilized proteins included 9 proteins that have been previously connected to cancer chemoresistance. Over-representation analysis (ORA) of all the differentially stabilized proteins identified here, revealed novel pathways related to oxaliplatin resistance. Compared to conventional protein expression level analyses, which were also performed on the cell lines and PDXs, the stability profiling techniques identified novel proteins and pathways and provided new insight on the molecular basis of oxaliplatin resistance. Our results suggest that protein stability profiling techniques are complementary to expression level analyses for identifying biomarkers and understanding molecular mechanisms associated with oxaliplatin chemoresistance in CRC and disease phenotypes in general.

2023-04-28 | PXD036298 | Pride

Prognostic Significance of Dual-Specificity Phosphatase 23 Expression in Acute Myeloid Leukemia.

Project description:BackgroundRecently, an increasing number of studies have suggested dual-specificity phosphatase 23 (DUSP23) is a critical factor in the development of diffuse connective tissue disease and may be a valuable biomarker for primary human cancers. However, there is a lack of comprehensive studies on the prognostic significance of DUSP23 expression in acute myeloid leukemia (AML).MethodsRNA sequencing data from The Cancer Genome Atlas (TCGA) (AML = 173), Genotype-Tissue Expression (GTEx) (healthy controls = 70) and GEO (AML = 461, healthy controls = 76) databases were used to compare DUSP23 expression between AML patients and healthy controls. The overall survival (OS) of DUSP23 in AML was evaluated using Kaplan-Meier Cox regression. Furthermore, univariate Cox regression and multivariate Cox regression analysis were used to determine whether DUSP23 was an independent prognostic factor for AML. We then verified the expression level and prognostic significance of DUSP23 in our cohort (AML = 128, healthy controls = 31). In addition, functional enrichment analysis of DUSP23-related DEGs was performed through gene set enrichment analysis (GSEA) and protein-protein interaction (PPI) network analysis.ResultsThe expression level of DUSP23 is significantly higher in AML patients than in healthy controls in TCGA, GTEx, GEO databases and our cohort. By multivariate analysis, high expression of DUSP23 is a poor prognostic indicator of OS in the TCGA database. Next, we verified the role of DUSP23 as an adverse prognostic biomarker in our cohort. Enrichment analysis of related genes showed that DUSP23 may regulate important signal pathways in hematological tumors including the MAPK pathways. It is suggested by the PPI network that DUSP23, along with IMP3, MRPL4, MRPS12, POLR2L, and ATP5F1D may play a role in the process of AML.ConclusionThe study demonstrated high expression of DUSP23 could serve as a poor independent prognostic biomarker in AML.

| S-EPMC10859056 | biostudies-literature

Methylation of Dual Specificity Phosphatase 4 Controls Cell Differentiation

Project description:Methylation of Dual Specificity Phosphatase 4 Controls Cell Differentiation

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Comamonas sp. 23 strain:23

Project description:Comamonas sp. 23 strain:23 Genome sequencing

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Colletotrichum gloeosporioides 23 strain:23

Project description:Colletotrichum gloeosporioides 23 strain:23 Genome sequencing and assembly

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