Knocking down HMGN2 can inhibit the proliferation, migration, and invasion of lung adenocarcinoma cells
10.19405/j.cnki.issn1000-1492.2025.03.012
- Author:
Zhi Chen
1
;
Xiao Zhu
2
;
Fubao Xing
2
;
Chao Song
2
;
Yang Geng
2
;
Wei Wang
2
;
Lei Zhang
2
Author Information
1. Anhui Provincial Key Laboratory of Cancer Translational Medicine，Bengbu Medical University，Bengbu 233000; Dept of Thoracic Surgery，The First Affiliated Hospital of Bengbu Medical University，Bengbu 233000
2. Dept of Thoracic Surgery，The First Affiliated Hospital of Bengbu Medical University，Bengbu 233000
- Publication Type:Journal Article
- Keywords:
olorectal carcinoma;
GPR15;
FOXP3;
immunohistochemistry;
prognosis
- From:
Acta Universitatis Medicinalis Anhui
2025;60(3):472-479, 487
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To investigate the effects and underlying mechanisms of high mobility group nucleosome-binding domain protein 2(HMGN2) on lung adenocarcinoma cells.
Methods :This work first analyzed the association between HMGN2 and lung adenocarcinoma tissues using The Cancer Genome Atlas(TCGA) database. Lung adenocarcinoma tissues and adjacent normal tissues were collected to compare the differential expression levels of HMGN2. The expression of HMGN2 mRNA in lung adenocarcinoma cell lines A549 and NC-H1299 were detected by qRT-PCR and Western blot. HMGN2 expression was knocked down using si-RNA technology, with the control group transfected with an equivalent amount of NC-siRNA, and the si-RNA group transfected with si-HMGN2. Stable transfected cell lines were established based on si-RNA knockdown efficiency. The effects of HMGN2 knockdown on the growth, movement, and spread of lung adenocarcinoma cells were assessed using CCK-8, Transwell assays, scratch assays, colony formation assays, and EdU assays. Transcriptome sequencing analysis revealed pathways related to tumorigenesis associated with HMGN2. The relative expression levels of MAPK pathway proteins after HMGN2 knockdown were detected by Western blot.
Results : HMGN2 mRNA expression was significantly elevated in lung cancer tissues and lung adenocarcinoma cell lines(P<0.05). After HMGN2 knockdown, cell proliferation, migration, and invasion were significantly reduced(P<0.05), and the phosphorylation levels of the MAPK signaling pathway markedly decreased(P<0.05).
Conclusion :HMGN2 enhances the proliferation, migration, and invasion of lung adenocarcinoma cells, and its mechanism may be closely related to the activation of the MAPK signaling pathwayviaphosphorylation.
- Full text:2026012318052838112敲低HMGN2可抑制肺腺癌细胞的增殖、迁移和侵袭_陈直.pdf
