Identification and Functional Analysis of MYEOV, KCNN4, S100A16 and DDX60L in Pancreatic Ductal Adenocarcinoma
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE171486 | GEO | 2021/04/06
REPOSITORIES: GEO
Similar Datasets
Project description:Identification and Functional Analysis of MYEOV, KCNN4, S100A16 and DDX60L in Pancreatic Ductal Adenocarcinoma
| PRJNA719795 | ENA
Project description:PURPOSE. Myeloma Overexpressed gene (MYEOV) was initially identified as a gene amplified in several malignancies, and it was found to promote cell proliferation and metastasis. Our previous comparative RNA-seq and epigenetic analyses revealed high MYEOV levels in differentiated corneal epithelial cells and showed that MYEOV expression was epigenetically regulated by TET2. In the current study, we aimed to characterize further the expression and regulation of MYEOV in the human ocular surface epithelium. METHODS. MYEOV expression was examined by immunostaining and publicly available single-cell RNA-seq data. Gene knockdown (KD) of MYEOV and the regulators of corneal epithelial differentiation, PAX6 and KLF4, in in vitro-expanded corneal epithelial cells was performed by siRNA transfection. Protein expression levels were examined by Western blot. MYEOV KD cells were subjected to colony-forming assay and RNA-seq analysis. RESULTS. Human cornea immunostaining revealed high MYEOV expression in the nuclei of KRT12-positive differentiated corneal epithelial cells, while KRT13-positive differentiated conjunctival epithelial cells were MYEOV-negative. MYEOV expression was not detected in the other surface ectoderm-derived epithelia: epidermis and oral mucosa. Both PAX6 KD and KLF4 KD led to the reduction of MYEOV and KRT12 protein expression. MYEOV KD decreased colony-forming efficiency while afflicting limited global gene expression change. CONCLUSIONS. Our study revealed specific MYEOV expression in KRT12-positive corneal epithelial cells among surface ectoderm-derived epithelia. Similar to KRT12, MYEOV expression is regulated by PAX6 and KLF4. Functionally, MYEOV regulates cell proliferation of corneal epithelial cells.
2025-12-04 | GSE295973 | GEO
Project description:Pancreatic cancer (PC) remains a highly lethal malignancy worldwide. As metastasis and malignant proliferation are primarily responsible for poor clinical outcomes of PC, it is imminent to dig out the pivotal gene involved in the process as well as its underlying molecular mechanism. In this study, through analysis of TCGA and GTEx data, we found that the expression level of MYEOV was obviously increased in carcinoma tissues relative to healthy ones and associated with poor survival in PC patients. The elevated abundance of MYEOV was positively correlated with enhanced cell proliferation, invasion and migration in vivo and in vitro. The global transcriptome analysis of MYEOV-depleted PC cells revealed the downregulation of various genes involved in active cell proliferation, which indicated that MYEOV overexpression was critical for PC progression. MiRNA-seq analysis showed that MYEOV had a regulatory effect on the expression levels of miR-17-5p and miR-93-5p, depletion of which resulted in reduced cell proliferation, invasion and migration as observed in MYEOV-knockdown PC cells. Such effect was imposed by MYEOV through affecting enrichment of the transcription factor c-myc at the gene promoter regions of the two miRNAs. Furthermore, a complex containing MYEOV and MYC was confirmed to exist in cell nucleus, providing convictive evidence for the association of MYEOV with MYC. Together, these results suggested that the axis of MYEOV-MYC-miR-17/93-5p could be vital for PC progression and could act as a potential therapeutic target to interrupt cell proliferation which will benefit treatment and management of PC patients.
2022-01-01 | GSE143827 | GEO
Project description:Myeloma Overexpressed (MYEOV) is closely related to cell growth and differentiation in many cancer types. However, the role of this protein-coding gene in pancreatic ductal adenocarcinoma (PDAC) has rarely been investigated. In this study, we demonstrated that MYEOV was higher expressed in tumor tissues compared with adjacent normal pancreas tissues (ANPTs) both in mRNA and protein levels. We also performed bioinformatic analysis and found high MYEOV expression was positively correlated with tumor differentiation (P = 0.004), lymph node metastasis (P = 0.016) and TNM stage (P = 0.001). Moreover, Kaplan-Meier and Cox proportional-hazards analyses indicated that high MYEOV expression was significantly associated with poor survival in patients with PDAC and that MYEOV was an independent prognostic factor for overall survival in patients with PDAC. Geneset Enrichment Analysis (GSEA) result showed that high expression of MYEOV facilitates glycolysis of tumor cells in PDAC and validated in cellular assays. In conclusion, our results suggest that MYEOV acts as an oncogene in PDAC and can therefore serve as a biomarker for the prognosis of patients with PDAC.
| S-EPMC7469688 | biostudies-literature
Project description:Pancreatic cancer (PC) remains a highly lethal malignancy worldwide. As metastasis and malignant proliferation are primarily responsible for poor clinical outcomes of PC, it is imminent to dig out the pivotal gene involved in the process as well as its underlying molecular mechanism. In this study, through analysis of TCGA and GTEx data, we found that the expression level of MYEOV was obviously increased in carcinoma tissues relative to healthy ones and associated with poor survival in PC patients. The elevated abundance of MYEOV was positively correlated with enhanced cell proliferation, invasion and migration in vivo and in vitro. The global transcriptome analysis of MYEOV-depleted PC cells revealed the downregulation of various genes involved in active cell proliferation, which indicated that MYEOV overexpression was critical for PC progression. MiRNA-seq analysis showed that MYEOV had a regulatory effect on the expression levels of miR-17-5p and miR-93-5p, depletion of which resulted in reduced cell proliferation, invasion and migration as observed in MYEOV-knockdown PC cells. Such effect was imposed by MYEOV through affecting enrichment of the transcription factor c-myc at the gene promoter regions of the two miRNAs. Furthermore, a complex containing MYEOV and MYC was confirmed to exist in cell nucleus, providing convictive evidence for the association of MYEOV with MYC. Together, these results suggested that the axis of MYEOV-MYC-miR-17/93-5p could be vital for PC progression and could act as a potential therapeutic target to interrupt cell proliferation which will benefit treatment and management of PC patients.
2021-12-29 | GSE143828 | GEO
Project description:To investigate the roles of MYEOV in lung cancer cell proliferation, we compared the expression profiles of A549 lung adenocarcinoma cell lines transfected with control siRNA and siMYEOV.
2017-06-28 | GSE65968 | GEO
Project description:To explore malignant phenotype related genes in Panc-1-CTC, we performed gene expression array analysis with Panc-1-CTC and Panc-1-Parent (Panc-1-P). As a result, TGFBI upregulation emerged as highly malignant feature for pancreatic ductal adenocarcinoma. Identification of malignant phenotype related genes in pancreatic ductal adenocarcinoma
2018-08-24 | GSE118556 | GEO
Project description:NO performs its biological roles mainly through protein S-nitrosylation, but pathogenic roles of protein S-nitrosylation in PDAC remains largely unexplored. In this study, we identified large number of unique S-nitrosylation sites and proteins in PDAC patients and PANC-1 cells by a site-specific proteomics.
2020-05-26 | PXD012512 | Pride
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy worldwide. As metastasis and malignant progression are primarily responsible for the poor clinical outcomes of PDAC, identifying key genes involved in these processes and the underlying molecular mechanisms of PDAC is vital. In this study, by analyzing TCGA PDAC data and matched GTEx data, we found that MYEOV expression is associated with poor survival in PDAC patients and higher in carcinoma tissues than in healthy tissues. Elevated levels of MYEOV led to enhanced cell proliferation, invasion and migration in vitro and in vivo. Transcriptome analysis results revealed that MYEOV mediates global alterations in gene expression profiles in PDAC cells. MiRNA-seq analysis showed that MYEOV regulates the expression levels of miR-17-5p and miR-93-5p, and its depletion resulted in reduced cell proliferation, invasion and migration, as observed in MYEOV-knockdown PDAC cells. These effects are likely due to the ability of MYEOV to regulate enrichment of the transcription factor MYC at the gene promoter regions of the two miRNAs. Furthermore, we identified a complex containing MYEOV and MYC in the nucleus, providing additional evidence for the association of MYEOV with MYC. Taken together, our results suggest that MYEOV promotes oncogenic miR-17/93-5p expression by associating with MYC, contributing to PDAC progression.
| S-EPMC8688437 | biostudies-literature
Project description:To reveal the molecular mechanisms underlying TQ tratment on cell proliferation, we performed circRNA-seq analysis on human PDAC cell cultures (MiaPaCa2 and Panc1 cells).
2025-09-09 | GSE307438 | GEO