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
Cervical cancer ranks second in the major causes of cancer-relevant death in female population worldwide. It is extensively reported that lncRNAs are implicated in biological activities of diverse cancers. LncRNA PTENP1 has been recently reported as a tumor suppressor in several malignancies. However, the pathophysiological function and the potential regulatory mechanism of PTENP1 in cervical cancer have never been studied. In this research, PTENP1 was pronouncedly downregulated in cervical cancer tissues, and low PTENP1 level was tightly linked to advanced stage and poor prognosis in cervical cancer. Overexpressing PTENP1 inhibited cervical cancer progression by suppressing cell growth, motility and epithelial-to-mesenchymal transition (EMT). PTENP1 was confirmed to decoy miR-27a-3p to upregulate EGR1 expression in cervical cancer cells. Additionally, EGR1 knockdown reversed the repressive effect of PTENP1 overexpression on cervical cancer progression. In a word, current study was the first to uncover the biological functions of PTENP1 as well as its modulatory mechanism in cervical cancer, which may offer a new potent target for treating patients with cervical cancer.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1038/s41434-020-00189-8 | DOI Listing |
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