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: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
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
N-methyladenosine (mA) modification is the most common epitranscriptomic modification in eukaryotic RNA and has garnered extensive attention in the context of breast cancer research. The mA modification significantly impacts tumorigenesis and tumor progression by regulating RNA stability, splicing, translation, and degradation. In this review we summarize recent advances in understanding the roles of mA modification in the mechanisms underlying angiogenesis and vasculogenic mimicry in breast cancer. We review how mA modification and associated transcripts influence relevant factors by affecting key factors and signaling pathways, highlighting the interactions among mA "writers," "erasers," and "readers," and their overall impact on tumor angiogenesis and vasculogenic mimicry, as well as potential new therapeutic targets.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.pbiomolbio.2024.12.003 | DOI Listing |
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