Asset Details
Do you wish to reserve the book?
HOPX hypermethylation promotes metastasis via activating SNAIL transcription in nasopharyngeal carcinoma
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
HOPX hypermethylation promotes metastasis via activating SNAIL transcription in nasopharyngeal carcinoma
Do you wish to request the book?
HOPX hypermethylation promotes metastasis via activating SNAIL transcription in nasopharyngeal carcinoma
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
HOPX hypermethylation promotes metastasis via activating SNAIL transcription in nasopharyngeal carcinoma
2017
Overview
Nasopharyngeal carcinoma (NPC) is characterized by a high rate of local invasion and early distant metastasis. Increasing evidence indicates that epigenetic abnormalities play important roles in NPC development. However, the epigenetic mechanisms underlying NPC metastasis remain unclear. Here we investigate aberrantly methylated transcription factors in NPC tissues, and we identify the
HOP
homeobox
HOPX
as the most significantly hypermethylated gene. Consistently, we find that HOXP expression is downregulated in NPC tissues and NPC cell lines. Restoring HOPX expression suppresses metastasis and enhances chemosensitivity of NPC cells. These effects are mediated by HOPX-mediated epigenetic silencing of
SNAIL
transcription through the enhancement of histone H3K9 deacetylation in the
SNAIL
promoter. Moreover, we find that patients with high methylation levels of
HOPX
exhibit poor clinical outcomes in both the training and validation cohorts. In summary,
HOPX
acts as a tumour suppressor via the epigenetic regulation of
SNAIL
transcription, which provides a novel prognostic biomarker for NPC metastasis and therapeutic target for NPC treatment.
HOPX is a transcription factor epigenetically silenced in several cancers. Here the authors, by analysing methylation profiles, identify HOPX as a suppressor of metastasis in nasopharyngeal carcinoma: mechanistically HOPX inhibits
SNAIL
transcription through deacetylation-mediated silencing.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/51
/ 14/19
/ 14/63
/ 38/1
/ 38/15
/ 64/60
/ 82/58
/ Animals
/ Cancer
/ Female
/ Gene Expression Regulation, Neoplastic
/ Genes
/ Genomes
/ Homeodomain Proteins - genetics
/ Humanities and Social Sciences
/ Humans
/ Nasopharyngeal Neoplasms - genetics
/ Nasopharyngeal Neoplasms - metabolism
/ Nasopharyngeal Neoplasms - pathology
/ Oncology
/ Promoter Regions, Genetic - genetics
/ Science
/ Snail Family Transcription Factors - genetics
