| Item type |
学位論文 / Thesis or Dissertation(1) |
| 公開日 |
2015-03-16 |
| タイトル |
|
|
タイトル |
Epigenetic alterations of the keratin 13 gene in oral squamous cell carcinoma. |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| キーワード |
|
|
言語 |
en |
|
主題 |
Keratin 13 (KRT13) |
| キーワード |
|
|
言語 |
en |
|
主題 |
Oral squamous cell carcinoma (OSCC) |
| キーワード |
|
|
言語 |
en |
|
主題 |
Polycomb repressive complex 2 (PRC2) |
| キーワード |
|
|
言語 |
en |
|
主題 |
Gene silencing |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_db06 |
|
資源タイプ |
doctoral thesis |
| アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 著者 |
Naganuma, Kaori
Hatta, Mitsutoki
Ikebe, Tetsuro
Yamazaki, Jun
|
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
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. |
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
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). |
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
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. |
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
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. |
| 学位名 |
|
|
学位名 |
博士（歯学） |
| 学位授与大学 |
|
|
|
学位授与機関識別子 |
37114 |
|
|
学位授与機関名 |
福岡歯科大学 |
| 学位授与年度 |
|
|
内容記述 |
2014年度 |
| 学位授与年月日 |
|
|
学位授与年月日 |
2015-03-14 |
| 報告番号 |
|
|
学位授与番号 |
甲第266号 |
| 情報源 |
|
|
|
関連名称 |
BMC Cancer. 2014 Dec 20;14:988. doi: 10.1186/1471-2407-14-988. |
| 関連サイト |
|
|
|
識別子タイプ |
URI |
|
|
関連識別子 |
http://www.biomedcentral.com/1471-2407/14/988 |
|
|
関連名称 |
BMC |
| 著者版フラグ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
甲第266号_論文(永沼) (1.6 MB)
