Effect of Shengmai Yin on Epithelial-Mesenchymal Transition of Nasopharyngeal Carcinoma Radioresistant Cells.
10.1007/s11655-022-3689-2
- Author:
Ze-Tai WANG
1
;
Yan PENG
1
;
Dan-Dan LOU
1
;
Si-Ying ZENG
1
;
Yuan-Chao ZHU
1
;
Ai-Wu LI
2
;
Ying LYU
2
;
Dao-Qi ZHU
1
;
Qin FAN
3
Author Information
1. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
2. Department of Traditional Chinese Medicine, Nanfang Hospital, Guangzhou, 510515, China.
3. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China. fqin@163.com.
- Publication Type:Journal Article
- Keywords:
Chinese medicine;
Shengmai Yin;
epithelial-mesenchymal transition;
lipocalin-2;
nasopharyngeal carcinoma;
radiation therapy
- MeSH:
Animals;
Humans;
Nasopharyngeal Carcinoma/genetics*;
Epithelial-Mesenchymal Transition;
Zebrafish;
Cell Proliferation;
Cell Line, Tumor;
Nasopharyngeal Neoplasms/radiotherapy*;
Cell Movement;
Gene Expression Regulation, Neoplastic
- From:
Chinese journal of integrative medicine
2023;29(8):691-698
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To investigate the mechanism by which Chinese medicine Shengmai Yin (SMY) reverses epithelial-mesenchymal transition (EMT) through lipocalin-2 (LCN2) in nasopharyngeal carcinoma (NPC) cells CNE-2R.
METHODS:Morphological changes in EMT in CNE-2R cells were observed under a microscope, and the expressions of EMT markers were detected using quantitative real-time PCR (RT-qPCR) and Western blot assays. Through the Gene Expression Omnibus dataset and text mining, LCN2 was found to be highly related to radiation resistance and EMT in NPC. The expressions of LCN2 and EMT markers following SMY treatment (50 and 100 µ g/mL) were detected by RT-qPCR and Western blot assays in vitro. Cell proliferation, migration, and invasion abilities were measured using colony formation, wound healing, and transwell invasion assays, respectively. The inhibitory effect of SMY in vivo was determined by observing a zebrafish xenograft model with a fluorescent label.
RESULTS:The CNE-2R cells showed EMT transition and high expression of LCN2, and the use of SMY (5, 10 and 20 µ g/mL) reduced the expression of LCN2 and reversed the EMT in the CNE-2R cells. Compared to that of the CNE-2R group, the proliferation, migration, and invasion abilities of SMY high-concentration group were weakened (P<0.05). Moreover, SMY mediated tumor growth and metastasis in a dose-dependent manner in a zebrafish xenograft model, which was consistent with the in vitro results.
CONCLUSIONS:SMY can reverse the EMT process of CNE-2R cells, which may be related to its inhibition of LCN2 expression. Therefore, LCN2 may be a potential diagnostic marker and therapeutic target in patients with NPC.
