Knockdown of RFC4 inhibits the cell proliferation of nasopharyngeal carcinoma in vitro and in vivo.
10.1007/s11684-022-0938-x
- Author:
Shuzhen GUAN
1
;
Lin FENG
2
;
Jinrui WEI
3
;
Guizhen WANG
4
;
Lichuan WU
5
Author Information
1. Medical College of Guangxi University, Nanning, 530004, China.
2. Department of Pathology, The First Medical Center of PLA General Hospital, Beijing, 100853, China.
3. Guangxi Scientific Research Center of Traditional Chinese Medicine, Guangxi University of Chinese Medicine, Nanning, 530200, China.
4. State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. gzwang@cicams.ac.cn.
5. Medical College of Guangxi University, Nanning, 530004, China. richard_wu@gxu.edu.cn.
- Publication Type:Journal Article
- Keywords:
RFC4;
WGCNA;
nasopharyngeal carcinoma;
proliferation
- MeSH:
Humans;
Nasopharyngeal Carcinoma/pathology*;
Carcinoma/pathology*;
Replication Protein C/metabolism*;
Nasopharyngeal Neoplasms/pathology*;
Cell Line, Tumor;
Cell Proliferation;
Gene Expression Regulation, Neoplastic;
Cell Movement
- From:
Frontiers of Medicine
2023;17(1):132-142
- CountryChina
- Language:English
-
Abstract:
Nasopharyngeal carcinoma (NPC) is a malignant tumor that mainly occurs in East and Southeast Asia. Although patients benefit from the main NPC treatments (e.g., radiotherapy and concurrent chemotherapy), persistent and recurrent diseases still occur in some NPC patients. Therefore, investigating the pathogenesis of NPC is of great clinical significance. In the present study, replication factor c subunit 4 (RFC4) is a key potential target involved in NPC progression via bioinformatics analysis. Furthermore, the expression and mechanism of RFC4 in NPC were investigated in vitro and in vivo. Our results revealed that RFC4 was more elevated in NPC tumor tissues than in normal tissues. RFC4 knockdown induced G2/M cell cycle arrest and inhibited NPC cell proliferation in vitro and in vivo. Interestingly, HOXA10 was confirmed as a downstream target of RFC4, and the overexpression of HOXA10 attenuated the silencing of RFC4-induced cell proliferation, colony formation inhibition, and cell cycle arrest. For the first time, this study reveals that RFC4 is required for NPC cell proliferation and may play a pivotal role in NPC tumorigenesis.
