Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
This study aimed to elucidate the relationship between and in bladder cancer and their underlying mechanism. Biological functions were evaluated using cell-counting kit 8 assay, 5-ethynyl-2'-deoxyuridine incorporation, wound healing and Transwell assays. RNA immunoprecipitation, RNA pull-down and chromatin immunoprecipitation were employed. A xenograft tumor model in nude mice was also conducted. and exhibited an inverse correlation. Downregulation of significantly suppressed bladder cancer cell proliferation, migration and invasion, which was reversed by overexpression. recruited DNA methyltransferases to the promoter region of , thereby triggering the methylation of the promoter to epigenetically suppress its expression. Our findings elucidate the machinery by which , stabilized by METTL3, exerts a promoter role in bladder cancer tumorigenesis by triggering methylation.
Download full-text PDF |
Source |
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http://dx.doi.org/10.2217/epi-2023-0062 | DOI Listing |
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