Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA106385 | ENA |
REPOSITORIES: ENA
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Project description:The protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. Studies have shown a relationship between PRL-1 and the expression or activity levels of various molecules involved in integrin-mediated cell signaling. These integrin-responsive players can promote re-arrangements in the actin cytoskeleton that are central to cell motility, invasion, and metastasis. Therefore, to investigate the effects of PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells, we used qRT-PCR to examine the expression levels of 184 genes which either were identified by microarray and proteomic analysis to be differentially expressed in response to PRL-1 or have known associations to integrin-mediated signaling, cytoskeletal remodeling, and/or cell motility. Total RNA was extracted from duplicate cultures of HEK293 cells stably overexpressing PRL-1 (HEK293-PRL-1) and HEK293 cells stably transfected with empty pcDNA4 vector (HEK293-Vector). Samples were analyzed using custom TaqMan Array 96-well Plates to examine the expression of 184 genes with known involvement in or association with signaling pathways related to integrin-mediated cell adhesion, cytoskeletal remodeling, and/or cell motility.
2013-07-30 | E-GEOD-42587 | biostudies-arrayexpress
Project description:The protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. Studies have shown a relationship between PRL-1 and the expression or activity levels of various molecules involved in integrin-mediated cell signaling. These integrin-responsive players can promote re-arrangements in the actin cytoskeleton that are central to cell motility, invasion, and metastasis. Therefore, to investigate the effects of PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells, we used qRT-PCR to examine the expression levels of 184 genes which either were identified by microarray and proteomic analysis to be differentially expressed in response to PRL-1 or have known associations to integrin-mediated signaling, cytoskeletal remodeling, and/or cell motility.
2013-07-30 | GSE42587 | GEO
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:HGF stimulates mitogenesis, motogenesis and morphogenesis in most epithelial target cells. Selective inhibition of HGF signaling blocks spontaneous metastasis, but not primary tumor growth, in the prostate adenocarcinoma derived PC3M cell xenograft model. To identify the HGF activated genes and pathways that contribute to cell motility and invasion, i.e. the HGF invasive program, expression profiling was performed on PC3M cells that were untreated or were treated with human HGF (hHGF), which drives all 3 primary activities, or with human HGF/NK2 (hNK2) or murine HGF (mHGF), which drive motility and invasion but not proliferation in human cells. Differences in gene expression profiles among these four groups were used to distiniguish between events associated with invasion (resulting from hNK2 or mHGF treatment) from those associated with the combination of invasion and proliferation (resulting from hHGF treatment). PC3M cells were left untreated or treated with hHGF, hNK2 or mHGF for 8, 16 or 32 hours prior to RNA extraction, cDNA preparation and array hybridization.
2015-08-25 | E-GEOD-71404 | biostudies-arrayexpress
Project description:Rho-GTPases are small GTP-binding proteins that contribute to the epithelial-to-mesenchymal transition by regulating several cellular processes including organization of the actin cytoskeleton, cell motility, transcription, and cell proliferation. Overexpression of RhoC-GTPases (RhoC) in breast cancer has been implicated in poor disease prognosis due to increased cancer cells invasion, migration, and motility, which warranted its consideration as a therapeutic target for inhibiting breast cancer metastasis. Using silencing RNA (siRNA) molecules to knockdown RhoC expression is a promising approach to inhibit breast cancer metastases.
2015-02-11 | ST000282 | MetabolomicsWorkbench
Project description:Breast cancer brain metastasis has been recognized as one of the central issues in breast cancer research. Elucidation of the process and pathway that mediate this step is expected to provide important clues for a better understanding of breast cancer metastasis. Increasing evidence suggests that the aberrant glycosylation patterns greatly contribute to the cell invasion and cancer metastasis. Herein, we combined next generation RNA sequencing with liquid chromatograph-tandem mass spectrometry based proteomic and N-glycomic analysis from five breast cancer cell lines and one brain cancer cell line to investigate the possible mechanism of breast cancer brain metastasis. 24763 genes were identified including 14551 differentially expressed genes across six cell lines while proteomic analysis allowed the quantitation of 1096 differentially expressed proteins with approximately 83.8% proteins’ regulation matching their gene expression change. The genes/proteins associated with cell movement were highlighted in the breast cancer brain metastasis. Integrin signaling pathway and the up-regulation of α-integrin (ITGA2, ITGA3) associated with the brain metastatic process was shown through Ingenuity Pathway Analysis (IPA). Overall 91 glycosylation genes were selected from transcriptomic data and all exhibited differential expression. 12 glycogenes showed unique expression in 231BR. The regulation of these genes could result in an activation prediction of sialylation function in 231BR by ingenuity pathway analysis. In agreement with the changes of glycogenes, 60 N-glycans out of 63 identified exhibited differential expression among cell lines. The correlation of glycogenes and glycans revealed the importance of sialylation and sialylated glycans in breast cancer brain metastasis. Highly sialylated glycans, which were up-regulated in brain seeking cell line 231BR, probably contributes to brain metastasis.
2020-05-26 | PXD010506 | Pride
Project description:Small cell lung cancer (SCLC) is the most aggressive lung cancer entity with an extremely limited therapeutic outcome. Most patients are diagnosed at an extensive stage. However, the molecular mechanisms driving SCLC invasion and metastasis remain largely elusive. We used an autochthonous SCLC mouse model and matched primary and metastatic SCLC patient samples to investigate the molecular characteristics of tumor metastasis. We demonstrate that tumor cell invasion and liver metastasis in SCLC are triggered by an Angiopoietin-2/Integrin beta-1-dependent pathway in tumor cells, mediated by focal adhesion kinase-Src kinase signaling. Strikingly, CRISPR-Cas9 knock out of Integrin beta-1 or blocking Integrin beta-1 signaling by an anti-Angiopoietin-2 treatment abrogates liver metastasis formation in vivo. Interestingly, analysis of a unique collection of matched primary and metastatic SCLC patient samples confirmed a strong increase of Integrin beta-1 in liver metastasis in comparison to the primary tumor. We further show that Angiopoietin-2 blockade combined with anti-VEGFR and PD-1-targeted treatment displays synergistic treatment effects in SCLC. Together, our data demonstrate a fundamental role of Angiopoietin-2/Integrin beta-1 signaling in SCLC cells for tumor cell invasion and liver metastasis and provide a new effective treatment strategy for patients with SCLC.
2024-03-28 | GSE262409 | GEO
Project description:We recently showed that inactivation of the WASF3/WAVE3 gene in breast cancer cells results in loss of cell motility and invasion in vitro and metastasis in vivo. To obtain a better understanding of molecular mechanisms of action of WASF3, we have established the stable WASF3 knockdown MDA-MB-231 cells using shRNA strategy. We used microarrays to detail the global programme of gene expression after silencing WASF3 and identified distinct classes of up or down-regulated genes associated with breast cancer cell migration and motility The three stable WASF3 knockdown single clones and three control clones were selected for RNA extraction and hybridization on Affymetrix microarrays. To identify altered gene expression patterns in the knockdown cells, we compared gene expression levels between three different knockdown and three different control clones.
2011-01-06 | E-GEOD-26462 | biostudies-arrayexpress
Project description:In this study, we sought to identify differentially expressed collagen/integrin genes in PNENs in order to understand the molecular mechanisms underlying the development of stroma-associated fibrosis for invasion and metastasis. We compared collagen/integrin gene expression profiling between PNE tumors (PNETs) and PNE carcinomas (PNECs) using a two-stage design. First, we used PCR Array System for 84 ECM-related genes, and among them, we found COL1A2, COL3A1, COL5A2, ITGA5, ITGAV, and ITGB1 functionally involved in the formation of the stroma-associated fibrosis among PNENs histological subtypes. Second, we examined the clinical association between the six collagen/integrin genes in tumor tissues from 24 patients with surgically excised PNENs.However, the pathological exam of their resected tissues demonstrated that 10 developed lymph node metastasis and 7 distant metastasis. We demonstrated and validated up regulation of the six fibrogenic genes in PNECs and down regulation in PNETs that were significantly associated with metastasis-free and overall survival (P<0.05). Our study implicates up regulation of fibrogenic genes as a critical molecular event leading to lymph node and distant metastasis in PNENs.
2021-08-04 | GSE181381 | GEO
Project description:HGF stimulates mitogenesis, motogenesis and morphogenesis in most epithelial target cells. Selective inhibition of HGF signaling blocks spontaneous metastasis, but not primary tumor growth, in the prostate adenocarcinoma derived PC3M cell xenograft model. To identify the HGF activated genes and pathways that contribute to cell motility and invasion, i.e. the HGF invasive program, expression profiling was performed on PC3M cells that were untreated or were treated with human HGF (hHGF), which drives all 3 primary activities, or with human HGF/NK2 (hNK2) or murine HGF (mHGF), which drive motility and invasion but not proliferation in human cells. Differences in gene expression profiles among these four groups were used to distiniguish between events associated with invasion (resulting from hNK2 or mHGF treatment) from those associated with the combination of invasion and proliferation (resulting from hHGF treatment).
2015-08-25 | GSE71404 | GEO