<i>ZNF350</i> promoter methylation accelerates colon cancer cell migration

Tanaka, Hiroki; Kuwano, Yuki; Nishikawa, Tatsuya; Rokutan, Kazuhito; Nishida, Kensei

doi:10.18632/oncotarget.26353

Cited by 12 publications

(13 citation statements)

References 43 publications

(62 reference statements)

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“…Numerous oncogenes and cancer-suppressor genes exhibit irregular expression, which is due to aberrant cytosine-phosphate-guanine (CpG)-island methylation in DNA regulatory regions rather than changes in the sequences[5]. For instance, the anti-oncogene ZNF350 undergoes epigenetic silencing due to hypermethylation of three sites in the promoter[6]. However, studies of DNA methylation in the individual genes remain inadequate.…”

Section: Introductionmentioning

confidence: 99%

Identification of differentially expressed genes regulated by methylation in colon cancer based on bioinformatics analysis

Yu¹,

Zhang²,

Dai³

2019

WJG

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BACKGROUND DNA methylation, acknowledged as a key modification in the field of epigenetics, regulates gene expression at the transcriptional level. Aberrant methylation in DNA regulatory regions could upregulate oncogenes and downregulate tumor suppressor genes without changing the sequences. However, studies of methylation in the control of gene expression are still inadequate. In the present research, we performed bioinformatics analysis to clarify the function of methylation and supply candidate methylation-related biomarkers and drivers for colon cancer. AIM To identify and analyze methylation-regulated differentially expressed genes (MeDEGs) in colon cancer by bioinformatics analysis. METHODS We downloaded RNA expression profiles, Illumina Human Methylation 450K BeadChip data, and clinical data of colon cancer from The Cancer Genome Atlas project. MeDEGs were identified by analyzing the gene expression and methylation levels using the edgeR and limma package in R software. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed in the DAVID database and KEGG Orthology-Based Annotation System 3.0, respectively. We then conducted Kaplan–Meier survival analysis to explore the relationship between methylation and expression and prognosis. Gene set enrichment analysis (GSEA) and investigation of protein-protein interactions (PPI) were performed to clarify the function of prognosis-related genes. RESULTS A total of 5 up-regulated and 81 down-regulated genes were identified as MeDEGs. GO and KEGG pathway analyses indicated that MeDEGs were enriched in multiple cancer-related terms. Furthermore, Kaplan–Meier survival analysis showed that the prognosis was negatively associated with the methylation status of glial cell-derived neurotrophic factor (GDNF) and reelin (RELN). In PPI networks, GDNF and RELN interact with neural cell adhesion molecule 1. Besides, GDNF can interact with GDNF family receptor alpha (GFRA1), GFRA2, GFRA3, and RET. RELN can interact with RAFAH1B1, disabled homolog 1, very low-density lipoprotein receptor, lipoprotein receptor-related protein 8, and NMDA 2B. Based on GSEA, hypermethylation of GDNF and RELN were both significantly associated with pathways including “RNA degradation,” “ribosome,” “mismatch repair,” “cell cycle” and “base excision repair.” CONCLUSION Aberrant DNA methylation plays an important role in colon cancer progression. MeDEGs that are associated with the overall survival of patients may be potential targets in tumor diagnosis and treatment.

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Section: Introductionmentioning

confidence: 99%

Identification of differentially expressed genes regulated by methylation in colon cancer based on bioinformatics analysis

Yu¹,

Zhang²,

Dai³

2019

WJG

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Section: Identification Of Mirnas Responsible For the High Migration mentioning

confidence: 99%

“…We have previously succeeded in isolating a subpopulation with accelerated baseline motility (migrated cells [MG] cells) and an immotile one (non-MG cells) from a colon cancer cell line (HCT116 p53 wild type) [13]. The MG cell subpopulation was composed of EMT intermediates with high expression levels of EMT marker genes ZEB1 and VIM [13]. In addition, MG cells expressed surface markers of colorectal cancer stem cells (ALDH1A1, CD24, POU5F1, SOX2, and SOX9) to a greater degree compared with non-MG cells [14] ( Figure S1).…”

Section: Identification Of Mirnas Responsible For the High Migration mentioning

confidence: 99%

“…A subpopulation with high migratory capacity, MG cells, were isolated by a transwell-based selection method [13]. In brief, for the isolation of a subpopulation with cell migration capacity, we established the following selection procedures using the transwell migration assay (the modified Boyden Chamber assay [37]).…”

Section: Cell Culture and Isolation Of A Subpopulation With High Cellmentioning

confidence: 99%

“…In this study, using a subpopulation with high migration capacity isolated from HCT116 cells using transwell apparatus [13], we sought to identify the miR-23b/27b/24 cluster, whose expression was upregulated in a subpopulation with cell migration capacity. The promoter assay of C9orf3, the host gene of the miR-23b/27b/24 cluster, revealed that E2F1 was involved in the regulation of the basic transcription activity of the short C9orf3 transcript.…”

Section: Introductionmentioning

confidence: 99%

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The MicroRNA-23b/27b/24 Cluster Facilitates Colon Cancer Cell Migration by Targeting FOXP2

Nishida

Kuwano

Rokutan

2020

Cancers

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Acquisition of cell migration capacity is an early and essential process in cancer development. The aim of this study was to identify microRNA gene expression networks that induced high migration capacity. Using colon cancer HCT116 cells subcloned by transwell-based migrated cell selection, microRNA array analysis was performed to examine the microRNA expression profile. Promoter activity and microRNA targets were assessed with luciferase reporters. Cell migration capacity was assessed by either the transwell or scratch assay. In isolated subpopulations with high migration capacity, the expression levels of the miR-23b/27b/24 cluster increased in accordance with the increased expression of the short C9orf3 transcript, a host gene of the miR-23b/27b/24 cluster. E2F1-binding sequences were involved in the basic transcription activity of the short C9orf3 expression, and E2F1-small-interfering (si)RNA treatment reduced the expression of both the C9orf3 and miR-23b/27b/24 clusters. Overexpression experiments showed that miR-23b and miR-27b promoted cell migration, but the opposite effect was observed with miR-24. Forkhead box P2 (FOXP2) mRNA and protein levels were reduced by both/either miR-23b and miR-27b. Furthermore, FOXP2 siRNA treatment significantly promoted cell migration. Our findings demonstrated a novel role of the miR-23b/27b/24 cluster in cell migration through targeting FOXP2, with potential implications for the development of microRNA-based therapy targeted at inhibiting cancer migration.

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Development of a kind of RG108-Fluorescein conjugates for detection of DNA methyltransferase 1 (DNMT1) in living cells

Ruan

Cheng

Gong

et al. 2020

Analytical Biochemistry

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ZNF350 promoter methylation accelerates colon cancer cell migration

Cited by 12 publications

References 43 publications

Identification of differentially expressed genes regulated by methylation in colon cancer based on bioinformatics analysis

Identification of differentially expressed genes regulated by methylation in colon cancer based on bioinformatics analysis

The MicroRNA-23b/27b/24 Cluster Facilitates Colon Cancer Cell Migration by Targeting FOXP2

Development of a kind of RG108-Fluorescein conjugates for detection of DNA methyltransferase 1 (DNMT1) in living cells

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