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
Lung adenocarcinoma (LUAD) is characterized by its aggressive nature and resistance to treatment. FAM107A is a tumor suppressor gene that has been found to possess inhibitory effects in several cancers, but its role in LUAD remains unclear. This study investigated the role of FAM107A in regulating LUAD cell growth, invasion and aerobic glycolysis and also investigated the potential underlying mechanisms. Our findings revealed that FAM107A is significantly downregulated in LUAD, and its overexpression inhibited LUAD cell growth and invasion. Furthermore, FAM107A overexpression suppressed the anaerobic phase of carbohydrate metabolism in LUAD cells. Mechanistically, FAM107A regulated the CRYAB/PI3K/AKT signaling pathway, thereby inhibiting tumor progression, and similar findings were confirmed in our in vivo mouse model. In conclusion, FAM107A can suppress LUAD progression by regulating the CRYAB/PI3K/AKT pathway and aerobic glycolysis, indicating its potential as therapeutic target for LUAD.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s10528-024-11006-x | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!