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Guanylate binding protein 5 accelerates gastric cancer progression via a JAK1-STAT1/GBP5/CXCL8 positive feedback loop

ABSTRACT: Guanylate binding protein 5 accelerates gastric cancer progression via a JAK1-STAT1/GBP5/CXCL8 positive feedback loop

PROVIDER: PRJNA897911 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22179063_1.fastq.gz	Fastqsanger.gz
	SRR22179063_2.fastq.gz	Fastqsanger.gz
	SRR22179064_1.fastq.gz	Fastqsanger.gz
	SRR22179064_2.fastq.gz	Fastqsanger.gz
	SRR22179065_1.fastq.gz	Fastqsanger.gz

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Guanylate binding protein 5 accelerates gastric cancer progression via a JAK1-STAT1/GBP5/CXCL8 positive feedback loop

Project description:To verify the role of GBP5 in GC progression, we established GBP5 -overexpressed MKN45 cells and control cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells with 3 duplicates each.

2024-10-29 | GSE217209 | GEO

The LIM protein AJUBA promotes colorectal cancer cell survival through suppression of JAK1/STAT1/IFIT2 network

Project description:Background and Aims: The LIM protein AJUBA participates in the regulation of cell adhesion, mitosis, DNA damage, cell differentiation, proliferation, migration and gene transcription, yet its roles in tumor development and progression are poorly defined. The aim is to determine the role of AJUBA in colorectal tumorigenesis. Methods: We performed data mining in Oncomine databases and immunohistochemistry (IHC) assays on 67 paired colorectal cancer (CRC) samples; we manipulated the AJUBA expression in SW-1116 and Caco-2 cells using specific shRNA and overexpression plasmids and performed assays for cell viability, cell cycle and apoptosis; we performed RNA-seq and qRT-PCR assays to identify genes regulated by AJUBA; we performed western blot, co-immunoprecipitation assays to study the interaction of AJUBA and JAK/STAT; Results: We discovered that AJUBA is highly expressed in CRC and promotes CRC cell growth in culture and in xenograted mice via an inhibition of apoptosis by repression of the IFIT2 gene. AJUBA specifically binds the FERM domain of JAK1 to dissociate JAK1 from the IFNγ recepter, resulted in inhibition of STAT1 phosporylation and concomitantly its nuclear translocation. Clinically, the level of AJUBA in CRC specimens is negatively correlated with the levels of IFIT2 and pSTAT1. Conclusion: Ajuba functions as a specific suppressor of the Interferon-activated JAK1/STAT1 signaling to promote colorectal cancer development via an inhibition of Interferon induced apoptosis.

2017-02-23 | GSE84902 | GEO

Profiling of transcriptional targets of Jak1 and Stat1 in proliferating and differentiating myoblasts

Project description:Profiling of transcriptional targets of Jak1 and Stat1 in proliferating and differentiating myoblasts

| PRJNA1090896 | ENA

Profiling of transcriptional targets of Jak1 and Stat1 in proliferating and differentiating myoblasts

Project description:Styxl2, a poorly characterized pseudophosphatase, was identified as a transcriptional target of the Jak1-Stat1 pathway during myoblast differentiation in culture. Styxl2 is specifically expressed in vertebrate striated muscles. By gene knockdown in zebrafish or genetic knockout in mice, we found that Styxl2 plays an essential role in maintaining sarcomere integrity in developing muscles. To further reveal the functions of Styxl2 in adult muscles, we generated two inducible knockout mouse models: one with Styxl2 being deleted in mature myofibers to assess its role in sarcomere maintenance, and the other in adult muscle satellite cells (MuSCs) to assess its role in de novo sarcomere assembly. We find that Styxl2 is not required for sarcomere maintenance but functions in de novo sarcomere assembly during injury-induced muscle regeneration. Mechanistically, Styxl2 interacts with non-muscle myosin IIs, enhances their ubiquitination, and targets them for autophagy-dependent degradation. Without Styxl2, the degradation of non-muscle myosin IIs is delayed, which leads to defective sarcomere assembly and force generation. Thus, Styxl2 promotes de novo sarcomere assembly by interacting with non-muscle myosin IIs and facilitating their autophagic degradation.

2024-03-31 | GSE262242 | GEO

JAK2V617F but not CALR mutations confer increased molecular responses to interferon-alpha via JAK1/STAT1 activation

Project description:JAK2V617F but not CALR mutations confer increased molecular responses to interferon-alpha via JAK1/STAT1 activation

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JAK-STAT1 as therapeutic target for EGFR deficiency-associated inflammation and scarring alopecia (scRNA-seq)

Project description:The hair follicle stem cell niche is an immune-privileged microenvironment, characterized by reduced antigen presentation, thus shielding against permanent immune-mediated tissue damage. In this study, we demonstrated the protective role of hair follicle-specific epidermal growth factor receptor (EGFR) against scarring hair follicle destruction. Mechanistically, disruption of EGFR signalling generated a cell-intrinsic hypersensitivity within the JAK-STAT1 pathway, which, synergistically with interferon gamma expressing CD8 T-cell and NK-cell-mediated inflammation, compromised the stem cell niche. Hair follicle-specific genetic depletion of either JAK1/2 or STAT1 or therapeutic inhibition of JAK1/2 ameliorated the inflammation, restored skin barrier function and activated the residual stem cells to resume hair growth in mouse models of epidermal and hair follicle-specific EGFR deletion. Skin biopsies from EGFR inhibitor-treated and cicatricial alopecia patients indicated active STAT1 signalling and interferon target expression. Notably, a case study of folliculitis decalvans, characterized by progressive hair loss, scaling and perifollicular erythema, demonstrated successful treatment with JAK1/2 inhibition. Our findings offer molecular insights and present a mechanism-based therapeutic strategy for addressing chronic folliculitis associated with EGFR-inhibitor anti-cancer therapy and cicatricial alopecia.

2024-07-31 | GSE273572 | GEO

Transcription profiling of human JAK1 wild-type and JAK1 mutation-positive T cell acute lymphoblastic leukemia blasts

Project description:Aberrant signal transduction contributes substantially to leukemogenesis. The Janus kinase 1 (JAK1) gene encodes a cytoplasmic tyrosine kinase that noncovalently associates with a variety of cytokine receptors and plays a nonredundant role in lymphoid cell precursor proliferation, survival, and differentiation. Somatic mutations in JAK1 occur in individuals with acute lymphoblastic leukemia (ALL). JAK1 mutations were more prevalent among adult subjects with the T cell precursor ALL, where they accounted for 18% of cases, and were associated with advanced age at diagnosis, poor response to therapy, and overall prognosis; We used microarray to compare the gene expression profile of JAK1 mutation positive or negative ALL blasts Experiment Overall Design: Thawed or freshly isolated T-ALL cells (>90% blasts) were homogenized, total RNA was extracted and hybridized on Affymetrix microarrays

2009-10-02 | E-GEOD-18239 | biostudies-arrayexpress

JAK-STAT1 as therapeutic target for EGFR deficiency-associated inflammation and scarring alopecia (RNA-seq of HFSC)

2024-07-31 | GSE273571 | GEO

Selective inhibitors of JAK1 targeting a subtype-restricted allosteric cysteine

Project description:The JAK family of non-receptor tyrosine kinases includes four subtypes (JAK1, JAK2, JAK3, and TYK2) and is responsible for signal transduction downstream of diverse cytokine receptors. JAK inhibitors have emerged as important therapies for immuno(onc)ological disorders, but their use is limited by undesirable side effects presumed to arise from poor subtype selectivity, a common challenge for inhibitors targeting the ATP-binding pocket of kinases. Here, we describe the chemical proteomic discovery of a druggable allosteric cysteine present in the non-catalytic pseudokinase domain of JAK1 (C817) and TYK2 (C838), but absent from JAK2 or JAK3. Electrophilic compounds selectively engaging this site block JAK1-dependent transphosphorylation and cytokine signaling, while appearing to act largely as “silent” ligands for TYK2. Importantly, the allosteric JAK1 inhibitors do not impair JAK2-dependent cytokine signaling and are inactive in cells expressing a C817A JAK1 mutant. Our findings thus reveal an allosteric approach for inhibiting JAK1 with unprecedented subtype selectivity.

2023-07-20 | PXD031384 | Pride

THe role of CXCL8 in the mesenchymal state of glioblastoma stem cells

Project description:To determine the functional significance of the expression of CXCL8 in mesenchymal GSCs, we examined the effect of CXCL8 disruption with two non-overlapping small hairpin RNAs (shRNA) on the mesenchymal GSC maintenance. Silencing CXCL8 with two independent shRNAs significantly reduced CXCL8 expression on in mesenchymal GSCs (839 and 2907) .

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