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STK24 Promotes Progression of LUAD and Modulates the Immune Microenvironment

Authors :
Yadong Li
Yanhu Liu
Kun Wang
Dong Xue
Yiqin Huang
Zhenguo Tan
Yijiang Chen
Source :
Mediators of Inflammation, Vol 2023 (2023)
Publication Year :
2023
Publisher :
Hindawi Limited, 2023.

Abstract

Objective. Recent studies have shown that serine/threonine-protein kinase 24 (STK24) plays an important role in cancer development. However, the significance of STK24 in lung adenocarcinoma (LUAD) remains to be determined. This study is aimed at investigating the significance of STK24 in LUAD. Methods. STK24 was silenced and overexpressed by siRNAs and lentivirus, respectively. Cellular function was assessed by CCK8, colony formation, transwell, apoptosis, and cell cycle. mRNA and protein abundance was checked by qRT-PCR and WB assay, respectively. Luciferase reporter activity was evaluated to examine the regulation of KLF5 on STK24. Various public databases and tools were applied to investigate the immune function and clinical significance of STK24 in LUAD. Results. We found that STK24 was overexpressed in lung adenocarcinoma (LUAD) tissues. High expression of STK24 predicted poor survival of LUAD patients. In vitro, STK24 enhanced the proliferation and colony growth ability of A549 and H1299 cells. STK24 knockdown induced apoptosis and cell cycle arrest at G0/G1 phase. Furthermore, Krüppel-like factor 5 (KLF5) activated STK24 in lung cancer cells and tissues. Enhanced lung cancer cell growth and migration triggered by KLF5 could be reversed by silencing of STK24. Finally, the bioinformatics results showed that STK24 may be involved in the regulation of the immunoregulatory process of LUAD. Conclusion. KLF5 upregulation of STK24 contributes to cell proliferation and migration in LUAD. Moreover, STK24 may participate in the immunomodulatory process of LUAD. Targeting KLF5/STK24 axis may be a potential therapeutic strategy for LUAD.

Subjects

Subjects :
Pathology
RB1-214

Details

Language :
English
ISSN :
14661861
Volume :
2023
Database :
Directory of Open Access Journals
Journal :
Mediators of Inflammation
Publication Type :
Academic Journal
Accession number :
edsdoj.913d47d7947a459c875fa6641b456196
Document Type :
article
Full Text :
https://doi.org/10.1155/2023/8646088