GEO accession GSE301311 is currently private and is scheduled to be released on Sep 15, 2025.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1284801 | ENA |
REPOSITORIES: ENA
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Project description:Esophageal cancer , a malignant tumor occurring in the upper gastrointestinal tract, is the seventh most common cancer worldwide. Zinc finger proteins, the most abundant family of transcription factors in humans, play a crucial role in the initiation and progression of various malignant tumors. However, its function in esophageal cancer remains unclear. The present study aimed to elucidate the role of ZNF514 in the development and progression of esophageal cancer, and to investigate its underlying mechanism. RNA expression and protein levels of ZNF514 were assessed using reverse transcription-quantitative PCR and western blotting . To assess functional roles, multiple cellular assays were performed, including: 5-ethynyl-2’-deoxyuridine incorporation ; Cell Counting Kit-8 ; wound healing assays ; colony formation assays ; Transwell assays. Subsequently, Gene Ontology, Gene Set Enrichment Analysis, Kyoto Encyclopedia of Genes and Genomes analysis and Ingenuity Pathway Analysis were performed through transcriptomic analysis. In EC, ZNF514 exhibited high expression at both the mRNA and protein levels. Additionally, ZNF514 influenced the migration, invasion and proliferation of EC cells. Gene enrichment analyses and IPA demonstrated that ZNF514 knockdown significantly affected multiple signaling pathways, such as Fcγ receptors, the complement system, G-protein coupled receptors-related receptors, the Ribosomal S6 kinase pathway, RAS/MEK, PI3K/AKT, STAT3, Nucleotide Binding Oligomerization Domain Containing , and NF-κB pathways. The anti-cancer mechanisms induced by ZNF514 knockdown may be related to the enhancement of Fcγ receptor and complement system activation, as well as the inhibition of GPCR, RSK, RAS/MEK, PI3K/AKT, STAT3, NOD1/2 and NF-κB pathways.
2025-09-30 | GSE301311 | GEO
Project description:IRS2 Promotes Proliferation and Drives Invasion-Migration in SI-NETs.
| PRJNA1310538 | ENA
Project description:Objectives: Long non-coding RNAs (lncRNAs) have been shown to play important roles in the development and progression of cancer. However, functional lncRNAs and their downstream mechanisms are largely unknown in the molecular pathogenesis of esophageal adenocarcinoma (EAC) and its progression. Design: lncRNAs that are abnormally upregulated in EACs were identified by RNA-seq analysis, followed by quantitative RT-PCR (qRTPCR) validation using tissues from 31 EAC patients. Cell biological assays in combination with siRNA-mediated knockdown were performed in order to probe the functional relevance of these lncRNAs. Results: We discovered that a lncRNA, HNF1A-AS1, is markedly upregulated in human primary EACs relative to their corresponding normal esophageal tissues (mean fold change 7.2, p<0.01). We further discovered that HNF1A-AS1 knockdown significantly inhibited cell proliferation and anchorage independent growth, suppressed S-phase entry, and inhibited cell migration and invasion in multiple in vitro EAC models (p<0.05). A gene ontological analysis revealed that HNF1A-AS1 knockdown preferentially affected genes that are linked to assembly of chromatin and the nucleosome, a mechanism essential to cell cycle progression. The well-known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs (p<0.01). In order to identify novel oncogenic lncRNAs in esophageal adenocarcinogenesis, we carried out RNA-seq of a matched NE-BE-EAC tissue pair
2013-10-21 | E-GEOD-48240 | biostudies-arrayexpress
Project description:Targeting the Epigenome Reduces Keloid Fibroblast Cell Proliferation, Migration and Invasion
| PRJNA970758 | ENA
Project description:The invasion capacity is one of the hallmarks of glioblastoma (GBM) cells. We found that ODZ1 which is mainly expressed in fetal brain, plays a crucial role in the migration and proliferation of GBM stem-like cells (GSCs). Introduction of the entire ODZ1 or its intracellular fragment in ODZ1-deficient cells promotes migration and invasion in 2D and 3D substrates and in chicken embryo and mouse xenograft models. Moreover, ODZ1 increases the proliferation of GSCs in culture and generates bigger tumor masses in the brain of xenografted mice. Consistently, higher levels of ODZ1 are correlated with lower survival both in patients and in xenograft models. On note, ODZ1 promotes the transcriptional activation of RhoA and ODZ1-induced proliferation and invasion activities were blocked by inhibiting RhoA-ROCK axis. Overall, we describe a novel cancer-associated gene involved in the progression of glioblastoma, providing a putative prognostic marker and a new target for therapeutic strategies.
2018-02-01 | GSE65526 | GEO
Project description:MIR193BHG inhibits the proliferation, migration and invasion of trophoblasts by upregulating p53
| PRJNA1027746 | ENA
Project description:Esophageal cancer, one of the most prevalent cancers worldwide, frequently exhibits distant metastases. The adipokine visfatin has been implicated in cancer progression and metastasis. However, the mechanisms by which visfatin regulates motility in esophageal cancer remain unclear. Here, we found that visfatin levels are higher in metastatic esophageal cancer patients than in primary esophageal cancer patients. Visfatin stimulation enhances migration and invasion in esophageal cancer cells. miRNA sequencing results revealed that miR-3613-5p controls visfatin-induced cell motility. Visfatin promotes esophageal cancer cell migration by reducing miR-3613-5p expression and subsequently increasing VEZF1/VCAN production. The visfatin/miR-3613-5p axis exhibits a promising target for inhibiting esophageal cancer metastasis.
2025-06-09 | GSE298998 | GEO
Project description:Objectives: Long non-coding RNAs (lncRNAs) have been shown to play important roles in the development and progression of cancer. However, functional lncRNAs and their downstream mechanisms are largely unknown in the molecular pathogenesis of esophageal adenocarcinoma (EAC) and its progression. Design: lncRNAs that are abnormally upregulated in EACs were identified by RNA-seq analysis, followed by quantitative RT-PCR (qRTPCR) validation using tissues from 31 EAC patients. Cell biological assays in combination with siRNA-mediated knockdown were performed in order to probe the functional relevance of these lncRNAs. Results: We discovered that a lncRNA, HNF1A-AS1, is markedly upregulated in human primary EACs relative to their corresponding normal esophageal tissues (mean fold change 7.2, p<0.01). We further discovered that HNF1A-AS1 knockdown significantly inhibited cell proliferation and anchorage independent growth, suppressed S-phase entry, and inhibited cell migration and invasion in multiple in vitro EAC models (p<0.05). A gene ontological analysis revealed that HNF1A-AS1 knockdown preferentially affected genes that are linked to assembly of chromatin and the nucleosome, a mechanism essential to cell cycle progression. The well-known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs (p<0.01).
2013-10-21 | GSE48240 | GEO
Project description:Abnormal placentation is a fundamental cause of pregnancy complications including preeclampsia, miscarriage, and intrauterine growth restriction. Proliferation, differentiation, migration, and invasion are key properties of trophoblast cells that regulate trophoblast functions. Imbalance of these cellular processes is linked to placental pathologies. Using HTR-8/SVneo immortalized human trophoblast cells, we demonstrate that steroid receptor coactivator-2 (SRC-2), a transcriptional regulator of nuclear receptors, is essential for extravillous trophoblast cell proliferation, migration, and invasion. Genome-wide transcriptomics identified an SRC-2–dependent transcriptome in HTR-8/SVneo cells that includes a diverse spectrum of proteins involved in placental tissue development and function. To emphasize the utility of this transcriptomics data set, we demonstrate that WNT family member 9A (WNT9A) is not only a molecular target of SRC-2 but also crucial for maintaining many of the cellular properties of human extravillous trophoblast cells.
2025-07-29 | GSE278677 | GEO
Project description:I investigated the role of insulin receptor substrate 2 (IRS2) in small-intestinal neuroendocrine tumours (SI-NETs). Using SI-NET cell lines (STC-1 and Glu-tag), I found that IRS2 was significantly upregulated. IRS2 knockdown inhibited cellular proliferation, migration, and invasion, while its overexpression promoted these processes. For in vivo validation, I established stable IRS2-knockdown cell lines and performed xenograft experiments in nude mice. Transcriptomic profiling by RNA sequencing was conducted to identify downstream targets of IRS2 signaling.
2025-08-26 | GSE306367 | GEO