Epigenetic alterations of the keratin 13 gene in oral squamous cell carcinoma.

• Material Type: 博士論文
• Title: Epigenetic alterations of the keratin 13 gene in oral squamous cell carcinoma.
• Author/Editor: Naganuma, Kaori; Hatta, Mitsutoki; Ikebe, Tetsuro; Yamazaki, Jun
• Author Heading: Naganuma, Kaori; Hatta, Mitsutoki; Ikebe, Tetsuro; Yamazaki, Jun
• Publication Date: 2015-03-14
• Publication Date (W3CDTF): 2015-03-14
• Alternative Title: Epigenetic alterations of the keratin 13 gene in oral squamous cell carcinoma.
• Degree grantor/type: 福岡歯科大学
• Date Granted: 2015-03-14
• Date Granted (W3CDTF): 2015-03-14
• Dissertation Number: 甲第266号
• Degree Type: 博士（歯学）
• Conferring No. (Dissertation): 甲第266号
• Text Language Code: eng
• Subject Heading: Keratin 13 (KRT13); Oral squamous cell carcinoma (OSCC); Polycomb repressive complex 2 (PRC2); Gene silencing
• Target Audience: 一般
• Note (General): Epigenetic modifications play important roles in the regulation of gene expression determining cellular phenotype as well as various pathologies such as cancer. Although the loss of keratin 13 (KRT13) is reportedly linked to malignant transformation of oral epithelial cells, the molecular mechanisms through which KRT13 is repressed in oral squamous cell carcinoma (OSCC) remain unclear. The aim of this study is to identify the epigenetic alterations of the KRT13 gene in OSCCs.; We investigated KRT13 expression levels and chromatin modifications of the KRT13 promoter in the three OSCC cell lines (HSC4, HSC3, and SAS). The expression levels of KRT13 protein and mRNA were analyzed by western blotting and quantitative reverse-transcription polymerase chain reaction, respectively, and the localization of KRT13 protein was detected by immunofluorescence. DNA methylation and histone modifications in the KRT13 promoter were determined by bisulfite sequencing and chromatin immunoprecipitation (ChIP), respectively. For the pharmacological depletion of Polycomb repressive complex 2 (PRC2), cells were treated with 3-deazaneplanocin A (DZNep).; KRT13 expression was transcriptionally silenced in the HSC3 and SAS cells and post-transcriptionally repressed in the HSC4 cells, while the KRT13 promoter was hypermethylated in all of the three OSCC cell lines. ChIP analysis revealed that PRC2-mediated trimethylation of Lys 27 on histone H3 (H3K27me3) was increased in the KRT13 promoter in the HSC3 and SAS cells. Finally, we demonstrated that the treatment of SAS cells with DZNep reactivated the transcription of KRT13 gene.; Our data provide mechanistic insights into the epigenetic silencing of KRT13 genes in OSCC cells and might be useful for the development of diagnostic markers and novel therapeutic approaches against OSCCs.; BMC Cancer. 2014 Dec 20;14:988. doi: 10.1186/1471-2407-14-988.; BMC
• Persistent ID (NDL): info:ndljp/pid/9479208; https://dl.ndl.go.jp/pid/9479208
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2015-08-01T14:40:15+09:00
• Date Created (W3CDTF): 2015-03-16
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Original Material (URI): BMC Cancer. 2014 Dec 20;14:988. doi: 10.1186/1471-2407-14-988.; http://www.biomedcentral.com/1471-2407/14/988
• Periodical Title (URI): https://fdc.repo.nii.ac.jp/records/36
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

Table of Contents

2023-12-07 再収集

2023-12-07 再収集

2023-12-07 再収集

2024-01-29 再収集

2024-01-29 再収集