Whole human genome expression microarray for circSTK3-related genes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE222838 | GEO | 2023/01/18
REPOSITORIES: GEO
Similar Datasets
Project description:We performed a genome-wide analysis of lncRNA expression to identify novel targets for the further study of liver metastasis in CRC. Samples obtained from CRC patients were analyzed using Arraystar human 8Ã?60K lncRNA/mRNA v3.0 microarrays chips to find differentially expressed lncRNAs and mRNAs; The results were confirmed by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The differentially expressed lncRNAs and mRNAs were identified through fold-change filtering. Gene ontology (GO) and pathway analyses were performed using standard enrichment computational methods. Twelve primary CRC samples were obtained from six patients with CRC and liver metastasis (Exp G) and six patients with CRC without metastasis (Ctrl G).
2016-05-18 | E-GEOD-75050 | biostudies-arrayexpress
Project description:We performed a genome-wide analysis of lncRNA expression to identify novel targets for the further study of liver metastasis in CRC. Samples obtained from CRC patients were analyzed using Arraystar human 8×60K lncRNA/mRNA v3.0 microarrays chips to find differentially expressed lncRNAs and mRNAs; The results were confirmed by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The differentially expressed lncRNAs and mRNAs were identified through fold-change filtering. Gene ontology (GO) and pathway analyses were performed using standard enrichment computational methods.
2016-05-18 | GSE75050 | GEO
Project description:Background: Distant metastasis remains a major reason for the high recurrence and mortality of colorectal cancer (CRC). However, the underlying molecular mechanisms driving metastasis in CRC remain poorly understood. In this study, we investigated the mechanisms underlying the inhibitory effects of lipocalin-2 (LCN2) on CRC metastasis. Methods: We assessed the expression and clinical significance of LCN2 in human CRC specimens and CRC cell lines using, immunohistochemistry, and western blot analyses. We evaluated the migratory and invasive capabilities of CRC cells influenced by LCN2 using in vitro transwell assays and in vivo lung metastatic models. RNA sequencing and proteome analysis were employed to identify potential downstream targets of LCN2. Rescue experiments were conducted to further elucidate the potential mechanisms of LCN2 and its downstream effectors in CRC. Results: LCN2 exhibited high expression levels in human CRC tissues and an inverse correlation with N classification, advanced AJCC stages, and shorter overall survival. LCN2 expression independently predicted a more favorable outcome for CRC patients. Upregulation of LCN2 effectively suppressed CRC cell metastasis both in vitro and in vivo. Mechanistically, Transforming growth factor beta 1 (TGFB1) and C-X-C motif chemokine ligand 5 (CXCL5) were identified as downstream effectors of LCN2, with LCN2 inhibiting CRC metastasis through repression of the TGFB1/CXCL5 axis. Furthermore, either TGF-βR1 inhibitor SB431542 or CXCR2 antagonist SB225002 treatment moderately decreased the migratory and invasive capabilities of DLD-1-LV-shLCN2 cells, whereas the combination treatment of the two agents dramatically decreased the migratory and invasive capabilities of DLD-1-LV-shLCN2 cells. Conclusions: This study underscores LCN2 as an independent protective factor and prognostic biomarker for CRC patients. Combined treatment with the SB431542 and the SB225002 significantly attenuated LCN2-related CRC metastasis. Targeting the LCN2/TGFB1/CXCL5 axis emerges as a promising therapeutic strategy for managing LCN2-related metastatic CRC.
2025-04-14 | GSE294201 | GEO
Project description:Here, we aimed to study metastasis mechanisms using spatial proteomics applied to the KM12 cell model of metastasis. KM12 cells were metabolically labelled using SILAC. SILAC has been successfully used for the analysis of proteome turnover and for the identification of changes in proteome localization as a consequence of DNA damage.10,23-24 Subcellular fractionation of the KM12 cells into five subcellular fractions corresponding to cytoplasm (CEB), plasma, mitochondria and ER/golgi membranes (MEB), nuclear (NEB), chromatin-bound (NEB-CBP) and cytoskeletal proteins (PEB) contributed to clarify the molecular mechanisms underlying CRC metastasis. Protein abundance and localization were measured in parallel for the five separate subcellular fractions, providing a map draft of the spatially deregulated protein complexes and networks in CRC metastasis.
2021-11-23 | MSV000088431 | MassIVE
Project description:Isoform-specific expression patterns have been implicated in stress-related psychiatric disorders like major depressive disorder (MDD), yet the extent of their involvement and their interrelationships remain unclear. We constructed co-expression networks for individuals affected (n=210, 81% with depressive symptoms) and unaffected (n=95) by stress-related psychiatric disorders. We incorporated total gene expression (TE) and isoform ratio (IR) data and validated the inferred networks using advanced graph generation techniques. Our analysis revealed distinct network topology and structure between the two groups. Investigation of the 127 shared hubs (degree >= 10) found that these hubs exhibit co-regulatory patterns unique to each network. The affected individuals’ network also contained 61 hub nodes with a minimum absolute fold increase of two in connectivity compared to the unaffected individuals’ network. Notably, 49% of these hubs showed evidence for association with psychiatric disorders. Gene Ontology enrichment analysis revealed distinct biological processes associated with hubs, such as mRNA processing for affected and immune response and cell adhesion for unaffected individuals. Enrichment analysis of GWAS loci further supported these findings. Analysis of the isoform-specific nodes showed distinct protein-protein interactions compared to gene-level analysis.
2025-02-10 | GSE289144 | GEO
Project description:Distant metastasis is the main cause of death in patients with colorectal cancer (CRC). A better understanding of the mechanisms of metastasis can greatly improve the outcome of patients with CRC. Accumulating evidence suggests that circRNA plays pivotal roles in cancer progression and metastasis, especially acting as a miRNA sponge to regulate the expression of the target gene. Public database bioinformatics analysis found that miR-1825 was highly expressed in CRC tissues. In this study, miR-1825 was highly expressed in CRC tissues, which was positively correlated with lymph node metastasis and distant metastasis. In vitro and in vivo experiments confirmed that miR-1825 was positively correlated with the proliferation and migration of CRC cells. This event can be inhibited by circTBC1D22A. CircTBC1D22A can directly interact with miR-1825 and subsequently act as a miRNA sponge to regulate the expression of target gene ATG14, which collectively advances the autophagy-mediated progression and metastasis of CRC.
2024-01-11 | GSE252689 | GEO
Project description:Colorectal cancer (CRC) is one of the most common death-related cancers worldwide. Aberrant expression of oncogenes is regarded as a predominant factor in CRC development. In our study, we found that TYRO3 intracellular domain nuclear translocation promotes CRC cell proliferation, metastasis, and tumor progression. To identify downstream effector that transmits the cellular functions of nuclear TYRO3, we performed nuclear TYRO3 co-immunoprecipitation.
2023-05-10 | PXD029743 | Pride
Project description:We analyzed protein cargos of NSC sEVs from proliferating, resting and reactivating status by proteomics approaches. Our results revealed specific functional clusters of pathways in gene ontology annotations of differentially expressed proteins in three sources of exosomes. Furthermore, we showed the involvement of sEVs in maintaining quiescence, along with entering and exiting the G0 phase by applying an exosome inhibitor. Our findings highlighted the expression level changes of NSCs of sEV protein cargo at different proliferative conditions and further confirmed the involvement of sEVs in entering, maintaining and exiting quiescence of NSCs.
2021-10-27 | PXD027651 | JPOST Repository
Project description:To better understand the tumorigenesis and metastasis of human metastatic melanoma(MM) , we analyzed the transcriptomes of three cell lines that represent the three distinct stages of MM pathogenesis: the normal stage (HEMn), the onset of MM (A375), and the metastasis stage (A2085). Using the next generation sequencing (NGS) technology, we detected unsymmetrical expression of genes particularly in Chr9, 12, and 14 among three cell lines, an indication of the involvement of these genes in the tumorigenesis and metastasis of MM. These genes were assigned into 41 categories by their expression patterns and their biological functions were subsequently analyzed by Ingenuity Pathway Analysis software. In the top category associated with cancer, HIF1A, IL8, TERT, ONECUT1 and FOXA1 had direct interaction with the transcription factors or cytokines known to be involved in the tumorigenesis or metastasis in other malignant tumors. Our findings suggest that pathway about cytokines regulation in macrophages may play a more prominent role in the pathogenesis of MM. This study provides not only new targets for downstream mechanistic studies in the tumorigenesis and metastasis of MM, but also a new strategy to study the progression of other malignant cancers. Compare the transcriptome of 3 cell lines of human melanocyte/melanoma
2015-02-10 | E-GEOD-35704 | biostudies-arrayexpress
Project description:Objective We have previously shown that expression of the CEACAM1 long isoform (CC1-L) in metastatic colorectal cancer (CRC) cells results in significant inhibition of liver metastasis via Chemokine (C-C motif) Ligand 2 (CCL2) and Signal Transducer and Activator of Transcription 3 (STAT3) signaling. Yet, despite recent advances in identifying molecules involved in the CC1-L inhibition of metastasis, much remains to be elucidated regarding the molecular mechanisms orchestrating this pathway. Design We performed an untargeted transcript profiling and a phosphokinase screen between CC1-L-expressing and non-expressing (CT) CRC cells. Identified targets were validated in vitro and in vivo for their involvement in signaling and invasion or metastasis. We validated our conclusions in CRC patient cohorts for time to metastasis development and long-term survival. Results Untargeted transcript profiling revealed high Decorin (Dcn) expression in CC1-L-expressing cells versus CT cells. Decorin was detected at the peri-endothelial layers of large blood vessels and in liver stellate cells. In metastatic lesions, it was expressed in pericyte-like cells covering capillary endothelium. Phosphokinase differential screening revealed reduced Ephrin type-A receptor 2 (EphA2) expression and activity in CC1-L- versus CT-expressing cells. Treatment of CT cells with recombinant Dcn led to decreased migration and invasion and decreased EphA2-mediated Erk and Akt signaling. CRC patients exhibiting high CC1 and DCN expression, in combination with low EPHA2 expression, benefit from longer 10-year survival than those with high EPHA2 expression. Conclusion CC1-L expression in poorly differentiated CRC inhibits liver metastasis through increased Decorin expression and EphA2-mediated signaling. Quadriplicate samples of each mouse colon cancer cell lines (control cells versus those expressing either short or long isoform of CEACAM1) have been used for RNA extraction
2015-09-19 | E-GEOD-73208 | biostudies-arrayexpress