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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Background: Antisense transcript of the B-cell translocation gene 3 (ASBEL) is a highly conserved antisense non-coding RNA (ncRNA) and participates in a variety of biological processes. However, the ASBEL expression status in pancreatic ductal adenocarcinoma (PDAC) and its correlation with expression and tumor cell progression were not completely clear.
Objective: We conducted cell experiments and animal experiments to confirm that ASBEL plays a crucial role in the tumorigenesis of PDAC by targeting BTG3.
Methods: ASBEL regulation in PDAC tumorigenesis was evaluated using Western blotting, quantitative polymerase chain reaction, Cell Counting Kit-8 assay, flow cytometry, and cell transfection. We also evaluated the expression of ASBEL and in tumor tissues and cells using Western blotting and quantitative real-time polymerase chain reaction. Finally, we explored the role of ASBEL in tumor development by silencing or overexpressing gene in AsPC-1 or CFPAC-1 cells, respectively, and evaluated the antitumor activity in vivo using an antagonist.
Results: Our study revealed the expression of in all pancreatic cell lines. The expression level of in tumor tissues was found to be higher than that of paracarcinomatous tissues. ASBEL suppresses expression of , enhances proliferation and suppresses apoptosis, and promotes migration and invasion in pancreatic cancer cell. Antagonist regulates the expression of ASBEL in AsPC-1, and suppresses tumor growth in xenograft mouse model.
Conclusions: Our results indicate that may play a tumor-promoting factor in PDAC by targeting and could be as an important biomarker for PDAC treatment. (. 2023; 84:XXX-XXX).
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Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10130767 | PMC |
http://dx.doi.org/10.1016/j.curtheres.2023.100700 | DOI Listing |