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
Background: Head and neck squamous cell carcinoma (HNSCC) has attracted the attention of researchers as a result of its high incidence around the world. This malignancy occurs in the oral cavity, pharynx and larynx in most cases. A number of lncRNAs have been revealed to regulate the malignant neoplasia of several cancers. Nevertheless, the effects of lncRNA LINC00467 in HNSCC have not yet been reported.
Methods: The expression of LINC00467, miR-299-5p and ubiquitin specific protease-48 (USP48) in HNSCC cells was quantified by a quantitative reverse transcriptase-polymerase chain reaction. The influences of LINC00467 deficiency on HNSCC progression were reflected by cell counting kit-8, colony formation, ethynyl-2-deoxyuridine, wound healing and western blot assays. RIP and luciferase reporter assays were conducted to confirm the interaction among LINC00467, miR-299-5p and USP48.
Results: LINC00467 was considerably upregulated in HNSCC cells, and an absence of LINC00467 suppressed cell growth, cell migration and the epithelial-mesenchymal process in HNSCC. In addition, miR-299-5p expression was notably downregulated in HNSCC cells, and miR-299-5p could bind with LINC00467. Furthermore, USP48 was conspicuously overexpressed in HNSCC cells and capable of binding with miR-299-5p. LINC00467 could upregulate USP48 expression via sponging miR-299-5p. Finally, rescue assays proved that USP48 overexpression could compensate for the suppressive effects on HNSCC progression mediated by LINC00467 deficiency.
Conclusions: LINC00467 enhances HNSCC progression by serving as a sponge of miR-299-5p to increase USP48 expression.
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Source |
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http://dx.doi.org/10.1002/jgm.3184 | DOI Listing |
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