PHF5A Promotes Proliferation and Migration of Non-Small Cell Lung Cancer
by Regulating of PI3K/AKT Pathway.
10.3779/j.issn.1009-3419.2023.102.01
- Author:
Houhui WANG
1
;
Fanglei LIU
1
;
Chunxue BAI
1
;
Nuo XU
1
Author Information
1. Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
- Publication Type:Journal Article
- Keywords:
Lung neoplasms;
Migration;
PHF5A;
Proliferation
- MeSH:
Humans;
Carcinoma, Non-Small-Cell Lung/pathology*;
Lung Neoplasms/pathology*;
Proto-Oncogene Proteins c-akt/metabolism*;
Phosphatidylinositol 3-Kinases/metabolism*;
Cell Line, Tumor;
Cell Proliferation/genetics*;
Cell Movement/genetics*;
Gene Expression Regulation, Neoplastic;
Trans-Activators/genetics*;
RNA-Binding Proteins/metabolism*
- From:
Chinese Journal of Lung Cancer
2023;26(1):10-16
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:There have been many significant advances in the diagnosis and treatment of non-small cell lung cancer (NSCLC). However, the mechanism underlying the progression of NSCLC is still not clear. Plant homodomain finger-like domain-containing protein 5A (PHF5A) plays an important role in processes of chromatin remodeling, morphological development of tissues and organs and maintenance of stem cell pluripotency. This study aims to investigate the role of PHF5A in the proliferation and migration of NSCLC.
METHODS:A549 and PC-9 PHF5A overexpression cell lines were constructed. PHF5A expression was decreased in H292 and H1299 cells by using siRNA. Flow cytometry was used to detect the cell cycle. MTT assay and clone formation assay were used to examine the proliferative ability of NSCLC, while migration assay and wound healing assay were performed to evaluate the ability of migration. Western blot analysis was used to measure the expressions of PI3K, p-AKT and the associated downstream factors.
RESULTS:Up-regulation of PHF5A in A549 and PC-9 cells increased the proliferation rate, while down-regulation of PHF5A in H292 and H1299 cells inhibited the proliferation rate at 24 h, 48 h and 72 h (P<0.05). The metastatic ability was elevated in the PHF5A-overexpresion groups, while reduced in the PHF5A-down-regulation group (P<0.05). In addition, reduced expression of PHF5A induced cell cycle arrest at G1/S phase (P<0.05). Furthermore, decreased expression of PHF5A reduced the expression levels of PI3K, phosphorylation of AKT, c-Myc (P<0.05) and elevated the expression of p21 (P<0.05).
CONCLUSIONS:These results demonstrated that PHF5A may play an important role in progression of NSCLC by regulating the PI3K/AKT signaling pathway.
