Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1075
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3195
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
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This study is aimed to investigate the clinical significance and biological function of long non-coding RNA somatostatin receptor 5 antisense RNA 1 (SSTR5-AS1) in prostate cancer (PCa). Here, we found that SSTR5-AS1 expression was upregulated in PCa tissues compared with adjacent tissues using quantitative real time PCR analysis. The results from Chi-square test showed that increased SSTR5-AS1 expression levels were correlated with preoperative prostate specific antigen, tumor stage and lymph node metastasis. Kaplan-Meier survival curve described patients with high SSTR5-AS1 expression level showed poor survival. Univariate and multivariate cox regression analysis further identified SSTR5-AS1 expression as a poor independent prognostic factor for PCa patients. Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2'-deoxyuridine incorporation assay, wound-healing assay and Transwell assay were performed to investigate the functional role of SSTR5-AS1 in PCa cells. The in vitro results indicated that SSTR5-AS1 knockdown inhibited, while SSTR5-AS1 overexpression promoted the proliferation, migration, and invasion of PCa cells. At molecular level, SSTR5-AS1 knockdown downregulated the protein levels of proliferating cell nuclear antigen, N-cadherin and vimentin, and upregulated E-cadherin expression in PC-3 cells. SSTR5-AS1 overexpression obtained opposite results on these protein markers in DU145 cells. In conclusion, these findings indicated that SSTR5-AS1 promotes PCa cell behaviors, which might provide a potential therapeutic target for PCa patients.
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http://dx.doi.org/10.1615/CritRevEukaryotGeneExpr.2022042183 | DOI Listing |