scholarly journals Expression and gene regulation network of EAF2 in cervical cancer based on data mining

2020 ◽  
Author(s):  
Wei na Kong ◽  
Fan Guo ◽  
Yang chun Feng ◽  
Jie Lv ◽  
Jia hui Fan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cervical Cancer ◽  
Cancer Progression ◽  
Survival Data ◽  
Mammalian Cells ◽  
Gene Networks ◽  
Patient Survival ◽  
Regulation Of Gene Expression ◽  
Cervical Cancer Patient ◽  
Risk Of Cancer

Abstract Background: ELL-associated factor 2 (EAF2) plays an important role in transcription elongation and the regulation of gene expression in both mammalian cells as well as in lower eukaryotes concurrent . EAF2’s depletion has been demonstrated to enhance cell proliferation and greatly increase the risk of cancer. However, little is known about the expression and function of EAF2 in cervical cancer (CC) progression. Here, we comprehensively analyzed the expression of EAF2 and its clinical outcome in CC using publicly available cancer gene expression and patient survival data through various databases.Methods: We examined the differences of EAF2 expression between cancers and their normal tissues using the Oncomine, Gene expression Profiling Interactive Analysis 2 (GEPIA2), the Gene Expression across Normal and Tumor tissue 2 (GENT2) database and UALCAN databases. EAF2 expression was investigated from immunohistochemistry images using the Human Protein Atlas database. Copy number alterations (CNAs) and mutations of EAF2 were analyzed using cBioPortal. Kaplan–Meier analysis was used to predict the survival of EAF2 in CC. Analysis of the co-expression profile of EAF2 and the enrichment pathway of co-expression with EAF2 were revealed using LinkedOmics to explore the predicted signaling pathways. GeneMANIA visualize the gene networks and predict function of genes that GSEA identified as being enriched in CC: kinase LYN, mi-RNA133A, 133B and transcription factor OCT1. Results: We found that the expression of EAF2 decreased with the development of CC and significant upregulation of EAF2 is positively correlated with the overall survival (OS) of CC patients. The decrease of EAF2 gene expression may be partly due to promoter methylation and CNAs with the development of CC. Besides, EAF2 expression might be strongly positively correlated with the expression of IQCB1, ILDR1 and ASTE1, and may contribute to a signaling pathway in CC. Conclusion: Decreased EAF2 expression has negative clinical significance in the development of CC through the regulation of methylation, CNAs and related pathways. This suggests that EAF2 has potential as a therapeutic target for CC. Keywords: EAF2; cervical cancer; patient survival; clinical outcomes; cancer progression; multiomics analysis

scholarly journals High Expression of TTYH3 is Related to Poor Clinical Outcomes in Human Gastric Cancer

2019 ◽  
Vol 8 (11) ◽  
pp. 1762 ◽  
Author(s):  
Saha ◽  
Biswas ◽  
Gil ◽  
Cho
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cancer Progression ◽  
Survival Data ◽  
Chloride Channels ◽  
Patient Survival ◽  
Chloride Ion ◽  
Gene Expression Omnibus ◽  
Human Gastric Cancer ◽  
Normal Tissues

Ion channels play important roles in regulating various cellular processes and malignant transformation. Expressions of some chloride channels have been suggested to be associated with patient survival in gastric cancer (GC). However, little is known about the expression and function of TTYH3, a gene encoding a chloride ion channel, in cancer progression. Here, we comprehensively analyzed the expression of TTYH3 and its clinical outcome in GC using publicly available cancer gene expression and patient survival data through various databases. We examined the differences of TTYH3 expression between cancers and their normal tissues using the Oncomine, UALCAN, and GEO (Gene Expression Omnibus) databases. TTYH3 expression was investigated from immunohistochemistry images using the Human Protein Atlas database. Copy number alterations and mutations of TTYH3 were analyzed using cBioPortal. The co-expression profile of TTYH3 in GC was revealed using Oncomine. The gene ontology and pathway analyses were done using those co-expressed genes via the Enrichr tool to explore the predicted signaling pathways in GC. TTYH3 mRNA and protein levels in GC were significantly greater than those in normal tissue. Kaplan–Meier analysis revealed the upregulation of TTYH3 expression, which was significantly correlated with worse patient survival. Collectively, our data suggest that TTYH3 might be a potential prognostic marker for GC patients.

scholarly journals Study on the regulatory mechanism of EAF2 in the microenvironment of cervical cancer

2021 ◽  
Author(s):  
Fan Guo ◽  
Wei na Kong ◽  
Gang Zhao ◽  
Jie Lv ◽  
Jia hui Fan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Mammalian Cells ◽  
Regulatory Mechanism ◽  
Regulation Of Gene Expression ◽  
Enrichment Analysis ◽  
Kaplan Meier ◽  
Risk Of Cancer ◽  
Expression In Mammalian Cells ◽  
Kaplan Meier Plotter

Abstract Objective EAF2 plays an important role in transcription elongation and the regulation of gene expression in mammalian cells. EAF2’s depletion has been demonstrated to enhance cell proliferation and greatly increase the risk of cancer. Even so, its expression and prognostic role in cervical cancer (CC) remains controversial. Methods To solve this issue, we comprehensively investigated the role of EAF2 in CC through various databases including ONCOMINE, UALCAN, Kaplan-Meier Plotter and TIMER. Results In all, we found that the EAF2 was highly expressed in CC tissue and was significantly correlated with better patient survival. Among the CNAs, amplification was the dominant alteration. Then the co-expression profile and enrichment analysis of EAF2 were related to the potential signaling pathways. The function of genes such as Kinase LYN, mi-RNA133A-133B and transcription factor OCT1 were also enriched in CC. The positively relation EAF2 expression to 6 immune cells revealed that EAF2 expression may affect development of patients with CC partially due to immune infiltration. Conclusions Taken together, our data suggest that EAF2 might be a potential prognostic marker and therapeutic target for CC patients.

scholarly journals A more efficient RNAi inducible system for tight regulation of gene expression in mammalian cells and xenograft animals

RNA ◽  
2007 ◽  
Vol 13 (8) ◽  
pp. 1375-1383 ◽  
Author(s):  
J. Zhang ◽  
C. Wang ◽  
N. Ke ◽  
J. Bliesath ◽  
J. Chionis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammalian Cells ◽  
Regulation Of Gene Expression ◽  
Expression In Mammalian Cells

scholarly journals Cervical Cancer Development: Implications of HPV16 E6E7-NFX1-123 Regulated Genes

Cancers ◽  
2021 ◽  
Vol 13 (24) ◽  
pp. 6182
Author(s):  
Kevin M. Quist ◽  
Isaiah Solorzano ◽  
Sebastian O. Wendel ◽  
Sreenivasulu Chintala ◽  
Cen Wu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cervical Cancer ◽  
Disease Progression ◽  
Patient Survival ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Cell Models ◽  
Cervical Precancer ◽  
Regulatory Effects ◽  
Cervical Cancer Development

High-risk human papillomavirus (HR HPV) causes nearly all cervical cancers, half of which are due to HPV type 16 (HPV16). HPV16 oncoprotein E6 (16E6) binds to NFX1-123, and dysregulates gene expression, but their clinical implications are unknown. Additionally, HPV16 E7’s role has not been studied in concert with NFX1-123 and 16E6. HR HPVs express both oncogenes, and transformation requires their expression, so we sought to investigate the effect of E7 on gene expression. This study’s goal was to define gene expression profiles across cervical precancer and cancer stages, identify genes correlating with disease progression, assess patient survival, and validate findings in cell models. We analyzed NCBI GEO datasets containing transcriptomic data linked with cervical cancer stage and utilized LASSO analysis to identify cancer-driving genes. Keratinocytes expressing 16E6 and 16E7 (16E6E7) and exogenous NFX1-123 were tested for LASSO-identified gene expression. Ten out of nineteen genes correlated with disease progression, including CEBPD, NOTCH1, and KRT16, and affected survival. 16E6E7 in keratinocytes increased CEBPD, KRT16, and SLPI, and decreased NOTCH1. Exogenous NFX1-123 in 16E6E7 keratinocytes resulted in significantly increased CEBPD and NOTCH1, and reduced SLPI. This work demonstrates the clinical relevance of CEBPD, NOTCH1, KRT16, and SLPI, and shows the regulatory effects of 16E6E7 and NFX1-123.

scholarly journals LSD1: more than demethylation of histone lysine residues

2020 ◽  
Vol 52 (12) ◽  
pp. 1936-1947
Author(s):  
Bruno Perillo ◽  
Alfonso Tramontano ◽  
Antonio Pezone ◽  
Antimo Migliaccio
Keyword(s):  
Gene Expression ◽  
Cancer Progression ◽  
Regulation Of Gene Expression ◽  
Histone H3 ◽  
Histone Demethylase ◽  
Special Role ◽  
Histone H4 ◽  
Nonhistone Proteins ◽  
Lysine Residues ◽  
Demethylase Activity

AbstractLysine-specific histone demethylase 1 (LSD1) represents the first example of an identified nuclear protein with histone demethylase activity. In particular, it plays a special role in the epigenetic regulation of gene expression, as it removes methyl groups from mono- and dimethylated lysine 4 and/or lysine 9 on histone H3 (H3K4me1/2 and H3K9me1/2), behaving as a repressor or activator of gene expression, respectively. Moreover, it has been recently found to demethylate monomethylated and dimethylated lysine 20 in histone H4 and to contribute to the balance of several other methylated lysine residues in histone H3 (i.e., H3K27, H3K36, and H3K79). Furthermore, in recent years, a plethora of nonhistone proteins have been detected as targets of LSD1 activity, suggesting that this demethylase is a fundamental player in the regulation of multiple pathways triggered in several cellular processes, including cancer progression. In this review, we analyze the molecular mechanism by which LSD1 displays its dual effect on gene expression (related to the specific lysine target), placing final emphasis on the use of pharmacological inhibitors of its activity in future clinical studies to fight cancer.

Regulation of gene expression and cellular proliferation by histone H2A.ZThis paper is one of a selection of papers published in this Special Issue, entitled CSBMCB’s 51st Annual Meeting – Epigenetics and Chromatin Dynamics, and has undergone the Journal’s usual peer review process.

2009 ◽  
Vol 87 (1) ◽  
pp. 179-188 ◽  
Author(s):  
Amy Svotelis ◽  
Nicolas Gévry ◽  
Luc Gaudreau
Keyword(s):  
Gene Expression ◽  
Transcriptional Activation ◽  
Mammalian Cells ◽  
Cellular Proliferation ◽  
Replicative Senescence ◽  
Peer Review Process ◽  
Regulation Of Gene Expression ◽  
Histone Variants ◽  
Chromatin Dynamics ◽  
Cycle Arrest

The mammalian genome is organized into a structure of DNA and proteins known as chromatin. In general, chromatin presents a barrier to gene expression that is regulated by several pathways, namely by the incorporation of histone variants into the nucleosome. In yeast, H2A.Z is an H2A histone variant that is incorporated into nucleosomes as an H2A.Z/H2B dimer by the Swr1 complex and by the SRCAP and p400/Tip60 complexes in mammalian cells. H2A.Z has been associated with the poising of genes for transcriptional activation in the yeast model system, and is essential for development in higher eukaryotes. Recent studies in our laboratory have demonstrated a p400-dependent deposition of H2A.Z at the promoter of p21WAF1/CIP1, a consequence that prevents the activation of the gene by p53, thereby inhibiting p53-dependent replicative senescence, a form of cell-cycle arrest crucial in the prevention of carcinogenic transformation of cells. Moreover, H2A.Z is overexpressed in several different types of cancers, and its overexpression has been associated functionally with the proliferation state of cells. Therefore, we suggest that H2A.Z is an important regulator of gene expression, and its deregulation may lead to the increased proliferation of mammalian cells.

scholarly journals Integrative analysis of DNA methylation and gene expression identified cervical cancer-specific diagnostic biomarkers

2019 ◽  
Vol 4 (1) ◽  
Author(s):  
Wanxue Xu ◽  
Mengyao Xu ◽  
Longlong Wang ◽  
Wei Zhou ◽  
Rong Xiang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cervical Cancer ◽  
Dna Methylation ◽  
Regulation Of Gene Expression ◽  
Cervical Squamous Cell Carcinoma ◽  
Integrative Analysis ◽  
Machine Learning Techniques ◽  
Marker Genes ◽  
Normal Tissues ◽  
Candidate Set

AbstractCervical cancer is the leading cause of death among women with cancer worldwide. Here, we performed an integrative analysis of Illumina HumanMethylation450K and RNA-seq data from TCGA to identify cervical cancer-specific DNA methylation markers. We first identified differentially methylated and expressed genes and examined the correlation between DNA methylation and gene expression. The DNA methylation profiles of 12 types of cancers, including cervical cancer, were used to generate a candidate set, and machine-learning techniques were adopted to define the final cervical cancer-specific markers in the candidate set. Then, we assessed the protein levels of marker genes by immunohistochemistry by using tissue arrays containing 93 human cervical squamous cell carcinoma samples and cancer-adjacent normal tissues. Promoter methylation was negatively correlated with the local regulation of gene expression. In the distant regulation of gene expression, the methylation of hypermethylated genes was more likely to be negatively correlated with gene expression, while the methylation of hypomethylated genes was more likely to be positively correlated with gene expression. Moreover, we identified four cervical cancer-specific methylation markers, cg07211381 (RAB3C), cg12205729 (GABRA2), cg20708961 (ZNF257), and cg26490054 (SLC5A8), with 96.2% sensitivity and 95.2% specificity by using the tenfold cross-validation of TCGA data. The four markers could distinguish tumors from normal tissues with a 94.2, 100, 100, and 100% AUC in four independent validation sets from the GEO database. Overall, our study demonstrates the potential use of methylation markers in cervical cancer diagnosis and may boost the development of new epigenetic therapies.

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