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
Evidence from previous studies showed that the dysregulation of microRNA (miR) is frequently associated with tumor progression. The aberrant miR-210 expression has been identified in a variety of tumors. However, its biological roles in esophageal squamous cell carcinoma (ESCC) still need further elucidation. Thus, in the current study we explore the roles of miR-210 in ESCC progression. The findings of our study reveal that miR-210 is down-regulated in ESCC, which indicates poor prognosis and aggressive tumor progression. Moreover, miR-210 restoration was found to enhance ESCC viability, invasion, and migration abilities. F-Box only protein 31 (FBXO31) was confirmed to be one of the targets of miR-210 in ESCC cells. Results also revealed that miR-210 played crucial roles in regulating ESCC cell epithelial-mesenchymal transition (EMT) and Wnt/β-catenin signaling. In conclusion, data show that miR-210 serves as an anti-ESCC miR via down-regulation of FBXO31 and regulation of EMT and Wnt signaling, suggesting that the miR-210/FBXO31 axis may function as promising therapeutic targets and effective prognostic markers for ESCC patients.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7952796 | PMC |
http://dx.doi.org/10.1111/1759-7714.13860 | DOI Listing |
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