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SiRNA profiling if human MCF-7 cell line to investigate the role of FAK, dominant-negative FAK, FAK-CD and FAKsiRNA in MCF-7 human breast cancer cell tumorigenesis

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Vita Golubovskaya

PROVIDER: E-GEOD-11581 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The direct effect of focal adhesion kinase (FAK), dominant-negative FAK, FAK-CD and FAK siRNA on gene expression and human MCF-7 breast cancer cell tumorigenesis.

Golubovskaya Vita M VM Zheng Min M Zhang Li L Li Jian-Liang JL Cance William G WG

BMC cancer 20090812

<h4>Background</h4>Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that plays an important role in survival signaling. FAK has been shown to be overexpressed in breast cancer tumors at early stages of tumorigenesis.<h4>Methods</h4>To study the direct effect of FAK on breast tumorigenesis, we developed Tet-ON (tetracycline-inducible) system of MCF-7 breast cancer cells stably transfected with FAK or dominant-negative, C-terminal domain of FAK (FAK-CD), and also FAKsiRNA with silence ...[more]

PMID: 19671193

Similar Datasets

Role of FAK, dominant-negative FAK, FAK-CD and FAKsiRNA in MCF-7 human breast cancer cell tumorigenesis

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

Expression data from FAK null mouse embryonic fibroblasts treated with endothelin-1

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

ATAC-seq of squamous cell carcinoma cells varying in FAK status

Project description:Focal adhesion kinase (FAK) localizes to focal adhesions and is overexpressed in many cancers. FAK can also translocate to the nucleus, where it binds to, and regulates, several transcription factors, including MBD2, p53 and IL-33, to control gene expression by unknown mechanisms. We have used ATAC-seq to reveal that FAK controls chromatin accessibility at a subset of regulated genes. Integration of ATAC-seq and RNA-seq data showed that FAK-dependent chromatin accessibility is linked to differential gene expression, including of the FAK-regulated cytokine and transcriptional regulator interleukin-33 (Il33), which controls anti-tumor immunity. Analysis of the accessibility peaks on the Il33 gene promoter/enhancer regions revealed sequences for several transcription factors, including ETS and AP-1 motifs, and we show that c-Jun, a component of AP-1, regulates Il33 gene expression by binding to its enhancer in a FAK kinase-dependent manner. This work provides the first demonstration that FAK controls transcription via chromatin accessibility, identifying a novel mechanism by which nuclear FAK regulates biologically important gene expression.

2021-01-15 | GSE161022 | GEO

Effect of norepinephrine and focal adhesion kinase (FAK) knockdown in prostate cancer

Project description:Chronic stress is associated with hormonal alterations that are known to promote cancer progression. The stress hormone norepinephrine promotes migration and metastasis of prostate cancer cells. Focal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase which is phosphorylated during chronic stress or norepinephrine treatment. Here, we investigated how norepinephrine modulates the gene expression in Myc-CaP prostate cancer cell line. We also focused on the effect of FAK knockdown in norepinephrine-induced changes of the gene expression profile.

2018-08-29 | GSE119157 | GEO

Effect of norepinephrine and focal adhesion kinase (FAK) knockdown in prostate cancer

Project description:Effect of norepinephrine and focal adhesion kinase (FAK) knockdown in prostate cancer

| PRJNA488279 | ENA

Expression data from FAK null mouse embryonic fibroblasts treated with endothelin-1

2012-07-01 | GSE30356 | GEO

MiR-19a/miR-96-mediated low expression of KIF26A suppresses metastasis by regulating FAK pathway in gastric cancer

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

ERK5 suppression overcomes FAK inhibitor resistance in mutant KRAS-driven non-small cell lung cancer [p826_PND_A549]

Project description:Mutated KRAS serves as the oncogenic driver in 30% of non-small cell lung cancers (NSCLCs) and is associated with metastatic and therapy-resistant tumors. Focal Adhesion Kinase (FAK) acts as a mediator in sustaining KRAS-driven lung tumors, and although FAK inhibitors are currently undergoing clinical development, clinical data indicated that their efficacy in producing long-term anti-tumor responses is limited. Here we revealed two FAK interactors, extracellular-signal-regulated kinase 5 (ERK5) and cyclin-dependent kinase 5 (CDK5) as key players underlying FAK-mediated maintenance of KRAS mutant NSCLC. Inhibition of ERK5 and CDK5 synergistically suppressed FAK function, decreased proliferation and induced apoptosis owing to exacerbated ROS-induced DNA damage. Accordingly, concomitant pharmacological inhibition of ERK5 and CDK5 in a mouse model of KrasG12D-driven lung adenocarcinoma suppressed tumor progression and promoted cancer cell death. Cancer cells resistant to FAK inhibitors showed enhanced ERK5-FAK signaling dampening DNA damage. Notably, ERK5 inhibition prevents resistance to FAK inhibitors, significantly enhancing the efficacy of antitumor responses. Therefore, we propose ERK5 inhibition as a potential co-targeting strategy to counteract FAK inhibitor resistance in NSCLC.

2024-09-16 | GSE255643 | GEO

ERK5 suppression overcomes FAK inhibitor resistance in mutant KRAS-driven non-small cell lung cancer [p697_ERK5]

2024-09-16 | GSE255628 | GEO

Transcription profiling of mouse cranial neural crest cells of E11.5 wild type and FAK mutants (valle-affy-mouse-480721)

Project description:Cranial neural crest cells (NCC) give rise to the majority of the cartilage, bone, connective tissue, and sensory ganglia in the head, and also participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardiovascular development. Our preliminary results show that targeted deletion of focal adhesion kinase (FAK) in murine NCC results in cardiovascular and craniofacial alterations, resembling human congenital heart diseases The objective of this project is to elucidate the underlying mechanisms by which FAK mediates NCC function during development. Compare gene expression in cranial neural crest cells of E11.5 wild type and FAK mutants. FAK is a tyrosine kinase that transduces integrin and growth factor signaling pathways. Abnormal growth factor signaling leads to cardiovascular malformations caused by deficient cardiac NCC function. However, a direct role for FAK in NCC morphogenesis has not been demonstrated. We will test the hypothesis that FAK is a downstream target of essential growth factor signaling in cranial neural crest cells during development. 1) Generate E11.5 mouse embryos that are either control (FAK+/flox) or NCC specific FAK knockout (Wnt1Cre;FAKflox/flox). 2) Determine genotype by PCR. 3) Dissect head and torax from the different genotypes. 4) Obtain NCC from dissected tissue by magnetic cell sorting using p75 antibody. 5) Prepare total RNA from speciments. We will pool the NCC from 3 different embryos of the same genotype, and send total RNA to TGEN for probe preparation, hybridization and array result analysis.

2008-06-11 | E-GEOD-11149 | biostudies-arrayexpress

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