Identifying Bit1-regulated genes in the EC9706 cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE78813 | GEO | 2016/03/03
SECONDARY ACCESSION(S): PRJNA314029
REPOSITORIES: GEO
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Project description:To further verify the underlying functions of Bit1 in ESCC, therefore, in the present study, we examined Bit1 expression in a panel of ESCC cell lines, and investigated the effects of Bit1 knockdown on tumor growth, migration and invasion as well as cell apoptosis in ESCC, and further preliminarily elucidated the possible molecular mechanisms. All data presented herein suggest Bit1 may be a promising molecular target for the therapy of ESCC, and thus intervention of Bit1 may lead to better therapeutic outcomes for the patients with ESCC. To further verify the underlying functions of Bit1 in ESCC, therefore, in the present study, we examined Bit1 expression in a panel of ESCC cell lines, and investigated the effects of Bit1 knockdown on tumor growth, migration and invasion as well as cell apoptosis in ESCC, and further preliminarily elucidated the possible molecular mechanisms. All data presented herein suggest Bit1 may be a promising molecular target for the therapy of ESCC, and thus intervention of Bit1 may lead to better therapeutic outcomes for the patients with ESCC. EC9706 cells were harvested 72 h after transfection with pSilencer3.1-H1 -neo-Bit1-shRNA or pSilencer3.1-H1-neo-negative-shRNA. Approximate 1â??Ã?â??106 cells from each sample were subjected to gene microarray assay. Total RNA was extracted was extracted for analysis.
2016-03-03 | E-GEOD-78813 | biostudies-arrayexpress
Project description:Background & Aims: Esophageal squamous cell carcinoma (ESCC) is believed to arise from esophageal mucosa through accumulation of both genetic and epigenetic changes. DNA methylation is a critical epigenetic mechanism involved in key cellular processes and its deregulation has been linked to many human cancers, including ESCC. The aim of this study is to examine the global deregulation of methylation states in ESCC and identify potential early biomarkers. Conclusions: This is the first study to address methylation changes in ESCC in a large panel of genes. Methylome analysis is shown as a sensitive and powerful tool to identify molecular players in ESCC. These data should prove to be the reference for future studies identifying potential biomarkers and molecular targets of ESCC. We performed a bead array analysis of more than 800 cancer-related genes in a series of 10 ESCC samples, 10 matched surrounding tissues, and 4 esophageal mucosa from healthy individuals. Pyrosequencing was used for validation of DNA methylation changes in up to 106 patients and 27 controls.
2011-11-23 | E-GEOD-26784 | 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:Background & Aims: Esophageal squamous cell carcinoma (ESCC) is believed to arise from esophageal mucosa through accumulation of both genetic and epigenetic changes. DNA methylation is a critical epigenetic mechanism involved in key cellular processes and its deregulation has been linked to many human cancers, including ESCC. The aim of this study is to examine the global deregulation of methylation states in ESCC and identify potential early biomarkers. Conclusions: This is the first study to address methylation changes in ESCC in a large panel of genes. Methylome analysis is shown as a sensitive and powerful tool to identify molecular players in ESCC. These data should prove to be the reference for future studies identifying potential biomarkers and molecular targets of ESCC.
2011-11-23 | GSE26784 | GEO
Project description:METTL3 and METTL14 are considered to faithfully form the m6A writing complex in a 1:1 ratio, regulating the fate of mRNA by adding m6A modifications. However, recent studies have shown inconsistent expression and prognostic value of METTL3 and METTL14 in some tumors, suggesting that they may not be faithful in tumors. Pan-cancer analysis based on TCGA data reveals significant differences in expression, function, tumor burden correlation, and immune correlation between METTL3 and METTL14, especially in esophageal squamous cell carcinoma (ESCC). Knockdown of METTL3 significantly inhibits the cell proliferation in vitro and in vivo in ESCC EC109 cells, while the impact of METTL14 knockdown on proliferation is limited, and it cannot abolish the expression of METTL3 protein. mRNA-seq results indicate that METTL3 independently regulates the expression of 1615 genes, while only 776 genes are co-regulated by METTL3 and METTL14. Furthermore, through immunofluorescence co-localization, it is observed that METTL3 and METTL14 have certain inconsistencies in cellular localization. HPLC-MS results show that METTL3 independently binds to the Nop56p-associated pre-rRNA complex and mRNA splicing complex, separate from METTL14. Through bioinformatics and various omics studies, we have preliminarily discovered that METTL3 independently regulating tumor cell proliferation, and the participation in mRNA splicing may be a critical molecular mechanism. Our study provides an experimental basis and theoretical foundation for further understanding of the m6A writing complex and tumor therapy targeting METTL3.
2024-02-01 | PXD048886 | Pride
Project description:Esophageal squamous cell carcinoma (ESCC) is a common digestive tract malignant tumor with high incidence and dismal prognosis throughout the world. However, the reliable biomarkers for clinical diagnosis and the comprehensive protein signaling regulatory networks for ESCC remain to be further elucidated. The serum proteome may provide valuable clues for early diagnosis of ESCC and discovery of novel molecular insights. In the current study, an optimized proteomics approach was employed to discover novel serum-based biomarker panel for ESCC, as well as unveil abnormal signal pathways. Gene ontology (GO) enrichment analysis was done by Gene Set Enrichment Analysis (GSEA) or Metascape database, respectively. Pathway analysis was accomplished by GeneCards database. The correlation coefficient was assessed using Pearson and distance correlation analyses. Prioritized candidates were further verified in two independent validation sets by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC) staining. A total of 633 non-redundant proteins were identified in serum of patients with ESCC, of which 59 proteins displayed more than 1.5-fold increase, whereas 10 ones showed 1.5-fold decrease compared with healthy controls. Verification was performed for candidate biomarkers including ENO1, TPI1, PGAM1, S100A8/A9 and SAA1. Receiver operating characteristics (ROC) curve showed a biomarker panel composed of three protein molecules including S100A8/A9 and SAA1 with a high diagnostic sensitivity and specificity, the area under characteristic curve (AUC) is up to 91.4%. Differentially expressed proteins were subjected to functional enrichment analysis which uncovered the dysregulation of signaling pathways mainly involving in glycolysis, TLR4, HIF-1, Cori cycle, TCA cycle, folate metabolism, and platelet degranulation. More importantly, activated glycolysis and TLR4 pathways were strongly positively correlated with unfavorable clinicopathological TNM stages in ESCC.
2022-01-26 | PXD031287 |
Project description:ESCC (Esophageal squamous cell carcinoma) is a common malignant tumor with high morbidity and mortality. CircRNAs (Circular RNAs) play important roles in various cancers including ESCC, the role of circMAN1A2(CircRNA mannosidase alpha class 1A member 2) in ESCC has not been sufficiently elucidated. The purpose of this study is to explore the biological function and potential mechanism of circMAN1A2 in ESCC, so as to provide a solid theoretical basis for circRNAs as a new target for diagnosis and treatment of ESCC.
2022-10-17 | GSE215844 | GEO
Project description:Esophageal cancer remains a dominating cause of cancer-associated death and has shown a sharp increase of more than 6-fold increase rates all over the world. It is divided into two main pathological types: esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC). Though the treatment has been improved a lot, the prognosis is still very poor with overall survival rate at 5 year was 15%-25%. Elaiophylin is a novel autophagy inhibitor at the late stage, which is a C2 symmetric macrolides separated from Streptomyces niger. However, the function of it in esophageal cancer was never explored. EIF4B is an important component of eukaryotic transcription initiation complex, which can be recruited to the 5’ untranslated region (5’UTR) of the mRNA. In recent years, eIF4B was suggested to play an important role in the progression of a various cancer cells. In the study we presented here, we firstly confirmed that the Elaiophylin was a novel autophagy inhibitor in ESCC cells. Moreover, Elaiophylin can inhibit the proliferation and migration of ESCCs, and promotes apoptosis. Then, we using RNA-seq to identify the genes which were regulated by Elaiophylin and verify them by RT-qPCR assay. Finally, we found the activity of PI3K/AKT pathway was inhibited by Elaiophylin. And the mRNA and protein expression level of eIF4B was both downregulated by Elaiophylin. In order to further confirm whether eIF4B is a target of Elaiophylin, we transfected a EIF4B-OE plasmid to ESCC cells, and found that the eIF4B overexpression could block the effect which was resulted from Elaiophylin. And by transfecting a shRNA to ESCC cells, we found that knockdown of eIF4B could inhibit the proliferation and migration of ESCC cells and promotes apoptosis when compared with the control group. All the results suggest that Elaiophylin could inhibit the proliferation, invasion of ESCC cells and promote its apoptosis by targeting the eIF4B via PI3K/AKT signaling pathway. This result identified that the Elaiophylin might serve as a promising therapeutic medicine for esophageal cancer.
2022-03-25 | GSE171167 | GEO
Project description:As a novel post-translational modification of histone derived from lactate, lysine lactylation (Kla) links lactate metabolism to epigenetic regulation, playing a role in modulation of gene expression in tumor and immune microenvironment. Evidence so far indicates that HDAC1-3 can catalyze the removal of Kla. However, the regulated targets of HDACs for Kla and functional consequence remain elusive. Herein, we used an antibody-based proximity labeling approach to identify SIRT3 binding to histone H3K9la and catalytic removal of the lactylationoup. The molecular docking results further revealed the mechanism of the binding of Kla peptide to SIRT3. More importantly, SIRT3 can specifically modulate the gene transcription by regulating H3K9la, inhibiting the progression of esophageal cancer cells (ESCC). In conclusion, our work identifies the delactylase of H3K9la and reveal an H3K9la-mediated molecular mechanism catalyzed by SIRT3 for gene transcription regulation in ESCC, and our findings provide an opportunity to investigate the physiological significance of Kla and shed light on the unknown cellular mechanisms controlled by SIRT3.
2024-08-18 | GSE274648 | GEO
Project description:Background and aims: Cancer metastasis is the biggest obstacle to esophageal squamous cell carcinoma (ESCC) treatment. At present, understanding of its mechanism remains insufficient. Therefore, an in-depth exploration of the mechanisms of metastasis is crucial for early detection and intervention to reduce metastasis-related mortality. Methods: This study applied single-cell RNA sequencing analysis to investigate lung metastatic ESCC cells isolated from a pulmonary metastasis mouse model at multiple timepoints to characterize early metastatic microenvironment. Results: We identified a small population of parental ESCC KYSE30 cell line (Cluster S) resembled metastasis-initiating cells (MICs) because they could survive and colonize at lung metastatic sites. By comparing differential expression profiles between Cluster S and other subpopulations, we identified a panel of 7 metastasis-initiating signature genes (MIS), including CD44 and TACSTD2, to represent MICs of ESCC. Functional studies demonstrated that Cluster S cells (CD44high) exhibited significantly enhanced cell survival (resistances to oxidative stress and apoptosis), cell migration, invasion, stemness, and in vivo lung metastasis capabilities. Multiplex immunohistochemistry (mIHC) staining of 4 MISs (CD44, S100A14, RHOD, and TACSTD2) in ESCC cell lines and clinical samples found that differential MIS expression scores (dMISs) could predict lymph node metastasis, overall survival and risk of carcinothrombosis. GO and KEGG analyses revealed that CD44high cells were enriched in cell migration, organ development, stress responses, and neuron development, which might be related to the establishment of early metastatic microenvironment. Conclusion: This study identified CD44, S100A14, RHOD, and TACSTD2 as MISs to represent the MICs in ESCC populations and predict patient outcomes. Keywords: ESCC, metastasis-initiating cells, metastasis-initiating signatures, biomarker, scRNA-seq.
2024-08-21 | GSE249057 | GEO