Ontology highlight
ABSTRACT:
PROVIDER: PRJNA890330 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21901376_1.fastq.gz | Fastqsanger.gz | |||
| SRR21901376_2.fastq.gz | Fastqsanger.gz | |||
| SRR21901377_1.fastq.gz | Fastqsanger.gz | |||
| SRR21901377_2.fastq.gz | Fastqsanger.gz | |||
| SRR21901378_1.fastq.gz | Fastqsanger.gz |
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Project description:A Kinase Anchoring Proteins (AKAPs) that coordinate spatiotemporal signaling are increasingly implicated in cancer. Elevated AKAP2 protein correlates with an invasive phenotype in triple-negative breast cancer cell lines. A combination of biochemical, cellular, and omics approaches show that AKAP2 cytoskeleton and focal adhesion associated scaffolds contribute to the progression of basal-like triple-negative breast cancer. Proximity proteomics identifies AKAP2 as an element of focal adhesions in MDA-MB-231 cells. Molecular and immunofluorescent microscopy studies demonstrate that AKAP2 indirectly constrains focal adhesion kinase (FAK). Gene silencing of AKAP2 not only decreases FAK levels but also attenuates the phosphorylation of the cell motility adapter protein paxillin on Tyr118. Cell-derived xenograft studies in mice establish that AKAP2 is required for triple-negative breast cancer growth and metastasis, phenotypes that are linked to FAK action. These findings discover a new role for focal adhesion-associated AKAP2 in triple-negative breast cancer pathology.
2025-11-25 | GSE311243 | GEO
Project description:Gastric cancer (GC) is one of the most common malignant neoplasms. Invasion and metastasis are the main causes of GC-related deaths. Recently, kinesins were discovered to be involved in tumor development. The aim of this study was to elucidate the roles of kinesin superfamily protein 26A (KIF26A) in GC and its underlying molecular mechanism in regulating tumor invasion and metastasis. Using real-time quantitative polymerase chain reaction (qPCR) and immunohistochemistry (IHC), we showed that KIF26A expression was lower in GC tissues without lymph node metastasis (LNM) than in nontumorous gastric mucosa, and even lower in GC tissues with LNM than in GC tissues without LNM. Functional experiments showed that KIF26A inhibited migration and invasion of GC cells. We further identifified focal-adhesion kinase (FAK), phosphatidylinositol 3-kinase regulatory subunit alpha (PI3KR1), VAV3, Rac1 and p21-activated kinase 2, and β-PAK (PAK3) as downstream effectors of KIF26A in the focal-adhesion pathway, and we found that KIF26A could regulate FAK mRNA expression through inhibiting c-MYC by MAPK pathway. c-MYC could bind to the promoter of FAK and activate FAK transcription. Moreover, we found that KIF26A mediated inactivation of the focal-adhesion pathway could reduce the occurrence of the epithelial-to-mesenchymal transition (EMT) by increasing expression of E-cadherin and reducing that of Snail. Luciferase assays and Western blotting revealed that miR-19a and miR-96 negatively regulate KIF26A. Finally, we found that decreased expression of KIF26A has been positively correlated with histological differentiation, Lauren classifification, LNM, distal metastasis, and clinical stage, as well as poor survival in patients with GC. These data indicate that KIF26A could inhibit GC migration and invasion by regulating the focal adhesion pathway and repressing the occurrence of EMT.
2021-07-16 | GSE180148 | GEO
Project description:Hypertrophic scar (HTS) formation is characterized by exuberant fibroproliferation for reasons that remain poorly understood1. One important but often overlooked component of wound repair is mechanical force, which regulates reciprocal cell-matrix interactions through focal adhesion components including focal adhesion kinase (FAK)1,2. Here we report that FAK is activated following cutaneous injury and that this activation is potentiated by mechanical loading. Transgenic mice lacking fibroblast-specific FAK exhibit significantly less fibrosis in a preclinical model of HTS formation. Inflammatory pathways involving monocyte chemoattractant protein-1 (MCP-1), a chemokine highly implicated in human skin fibrosis3, are triggered following FAK activation, mechanistically linking physical force to fibrosis. Further, small molecule inhibition of FAK effectively abrogates fibroproliferative mechanisms in human cells and significantly reduces scar formation in vivo. Collectively, these findings establish a molecular basis for HTS formation based on the mechanical activation of fibroblast-specific FAK and demonstrate the therapeutic potential of targeted mechanomodulatory strategies.
2011-01-14 | GSE26390 | GEO
Project description:Hypertrophic scar (HTS) formation is characterized by exuberant fibroproliferation for reasons that remain poorly understood1. One important but often overlooked component of wound repair is mechanical force, which regulates reciprocal cell-matrix interactions through focal adhesion components including focal adhesion kinase (FAK)1,2. Here we report that FAK is activated following cutaneous injury and that this activation is potentiated by mechanical loading. Transgenic mice lacking fibroblast-specific FAK exhibit significantly less fibrosis in a preclinical model of HTS formation. Inflammatory pathways involving monocyte chemoattractant protein-1 (MCP-1), a chemokine highly implicated in human skin fibrosis3, are triggered following FAK activation, mechanistically linking physical force to fibrosis. Further, small molecule inhibition of FAK effectively abrogates fibroproliferative mechanisms in human cells and significantly reduces scar formation in vivo. Collectively, these findings establish a molecular basis for HTS formation based on the mechanical activation of fibroblast-specific FAK and demonstrate the therapeutic potential of targeted mechanomodulatory strategies. Wildtype murine tissue was harvested at either day 6 or 14 post-injury following 48 hours or 10 days of mechanical loading, respectively (n=4 mice per group per time point). Murine RNA was isolated, labeled, and hybridized to the GeneChip microarray according to the manufacturer’s protocols (Affymetrix, Santa Clara, CA, USA). Each gene in the microarray was represented by 20 oligonucleotide pairs, with each pair consisting of an oligonucleotide perfectly matched to the cDNA sequence, and a second oligonucleotide containing a single base mismatch. Raw microarray data (sample intensity files) were processed using GeneSpring GX 11.0 (Agilent Technologies Inc., Santa Clara, CA, USA).
2011-01-14 | E-GEOD-26390 | biostudies-arrayexpress
Project description:Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that plays an important role in proliferation, motility, adhesion, invasion, angiogenesis, and survival signaling. Focal adhesion kinase has been shown to be overexpressed in many types of tumors, including breast cancer at early stages of tumorigenesis. To study the biological role of FAK in breast tumorigenesis, we used FAKsiRNA to down-regulate FAK in MCF-7 cell lines. Experiment Overall Design: Eight samples were analyzed in MCF-7, MCF-7-Vector, MCF-7 control (luciferase) siRNA and FAKsiRNA#1, FAKsiRNA#2
2009-08-22 | E-GEOD-11581 | biostudies-arrayexpress
Project description:Obesity is a significant public health concern associated with increased infection risk, but the mechanisms remain unclear. Using a diet induced obesity mouse model, we investigate how obesity impacts urinary tract infection (UTI) susceptibility and bladder urothelial defenses. High fat diet-fed female and male C57BL/6 mice exhibit increased susceptibility to uropathogenic E. coli (UPEC) following experimental UTI. Transcriptomic analysis of bladder urothelial cells reveals sex-specific gene expression changes, but both sexes share activation of focal adhesion and extracellular matrix signaling. Western blot and immunostaining confirm activation of focal adhesion kinase (FAK), a central component of the focal adhesion pathway, in the bladders of obese female and male mice. Mechanistically, primary human urothelial cells overexpressing FAK exhibit increased UPEC invasion. These findings demonstrate that obesity enhances UTI susceptibility and identify FAK as a conserved pathway disrupted by obesity, contributing to increased UPEC vulnerability.
2025-09-19 | GSE294660 | GEO
Project description:p130Cas (Cas, Crk-associated substrate) is an adaptor molecule composed of an N-terminal Src homology 3 (SH3) domain, a substrate domain (SD), and a C-terminal Src binding domain (SBD). The SH3 domain of Cas has been shown to associate with various signaling molecules, including focal adhesion kinase (FAK), but its role in cellular function remains unclear. To address this issue, we established and analyzed primary fibroblasts derived from mice expressing a truncated Cas lacking the exon 2 encoding the SH3 domain (Cas exon 2â/â). In comparison to wild-type (Cas exon 2+/+) cells, Cas exon 2â/â primary fibroblasts showed delayed migration in wound healing and reduced spreading on fibronectin (FN), which would be due to reduced complex formation of Cas exon 2â/â with FAK and CrkII and also to impaired localization of Cas exon 2â/â to focal adhesions on FN. In addition, to analyze downstream signaling pathway regulated by Cas exon 2, we compared gene expression profiles between Cas exon 2+/+ and Cas exon 2â/â cells by a microarray analysis. Interestingly, we found that Cas exon 2-deficiency upregulated expression of CXC Chemokine Receptor-4 (CXCR4), CC Chemokine Receptor-5 (CCR5), and thrombospondin 4, which are implicated in cell motility and adhesion. These results define the role of Cas SH3-encoding exon in cell motility, FAK/Cas/CrkII complex formation, recruitment of Cas to focal adhesions, and regulation of cell adhesion-associated gene expression in primary fibroblasts. Experiment Overall Design: RNA samples extracted from Cas exon 2+/+, Cas exon 2+/â, and Cas exon 2â/â fibroblasts (12.5dpc, two embryos for each genotype) were labeled and hybridized on Affymetrix microarray. Gene expression patterns of Cas exon 2â/â fibroblasts were compared with those of Cas exon 2+/+ and Cas exon 2+/â cells.
2008-06-16 | E-GEOD-8357 | biostudies-arrayexpress
Project description:Purpose: Esophageal squamous cell carcinoma (ESCC) is a serious malignant tumor, it affects human health. We analyzed the correlation between serum Stathmin levels and ESCC, further elucidated the molecular mechanisms how Stathmin promotes ESCC cell invasion and metastasis. Methods: Stathmin levels in ESCC and healthy control serum was detected by enzyme-linked immunosorbent assay (ELISA), and analyzed the clinical parameters. We established ESCC cells with Stathmin overexpression or knockdown, next evaluated the effects of Stathmin on invasion, metastasis and proliferation in ESCC. The expression levels of the integrin family, focal adhesion kinase (FAK) protein and extracellular signal-regulated kinase (ERK) were detected by immunoblotting. Results: Serum levels of Stathmin were significantly higher in ESCC and associated with lymph node metastasis, tumor stage and size. Furthermore, we found Stathmin promotes migration, invasion and proliferation of ESCC cells in vitro and in vivo. Further study confirmed that the activation of integrinα5β1/FAK/ERK pathway is increased in Stathmin overexpression cells, this pathway contribute to strengthen cell adhesion. Stathmin accelerates the cell motility by enhancing cell adhesion ability. Conclusion: Stathmin may be a potential biomarker for ESCC clinical detection, and it can promotes ESCC cell invasion and metastasis through the integrinα5β1/FAK/ERK pathway. The differentially expressed genes were analyzed by Human Transcriptome Array, and confirmed by RT-PCR.
2016-11-29 | GSE90578 | GEO
Project description:Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that plays an important role in proliferation, motility, adhesion, invasion, angiogenesis, and survival signaling. Focal adhesion kinase has been shown to be overexpressed in many types of tumors, including breast cancer at early stages of tumorigenesis. To study the biological role of FAK in breast tumorigenesis, we used FAKsiRNA to down-regulate FAK in MCF-7 cell lines.
2009-08-17 | GSE11581 | GEO
Project description:Endothelin-1 (ET-1) plays a critical role in connective tissue remodeling by fibroblasts during tissue repair and fibrosis. We investigated the molecular pathways in the transmission of ET-1 signals that lead to features of connective tissue remodeling, in particular the role of FAK (focal adhesion kinase). We used microarrays to investigated whether FAK is required for ET-1 to promote the global programme of gene expression underlying myofibroblast formation and identified distinct classes of up-regulated genes during this process. Genes whose induction by ET-1 required FAK Affymetrix Mouse Genome 430 2.0 GeneChips were used to identify differential gene expression changes bewteen samples.
2012-06-30 | E-GEOD-30356 | biostudies-arrayexpress