MYEOV as a novel biomarker for human non-small cell lung cancer
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE65968 | GEO | 2017/06/28
SECONDARY ACCESSION(S): PRJNA275608
REPOSITORIES: GEO
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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.
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Project description:siRNA of MYEOV, KCNN4, S100A16 and DDX60L treated MiaPaCa2 and PANC-1 cells were used for RNA-seq to identify the transcriptomic alterations.
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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: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.
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Project description:MYEOV is a novel marker of differentiated corneal epithelium
| PRJNA1256899 | ENA