Downregulation of MUC1 Inhibits Proliferation and Promotes Apoptosis by Inactivating NF-κB Signaling Pathway in Human Nasopharyngeal Carcinoma
- VernacularTitle:MUC1下调通过失活NF-κB通路抑制鼻咽癌细胞增殖并促进其凋亡
- Author:
Shou-Wu WU
1
;
Shao-Kun LIN
2
;
Zhong-Zhu NIAN
1
;
Xin-Wen WANG
3
;
Wei-Nian LIN
1
;
Li-Ming ZHUANG
1
;
Zhi-Sheng WU
1
;
Zhi-Wei HUANG
1
;
A-Min WANG
1
;
Ni-Li GAO
1
;
Jia-Wen CHEN
3
;
Wen-Ting YUAN
3
;
Kai-Xian LU
3
;
Jun LIAO
1
Author Information
- Publication Type:Journal Article
- Keywords: mucin 1; nasopharyngeal carcinoma; NF-κB signaling pathway; proliferation; apoptosis
- From: Progress in Biochemistry and Biophysics 2024;51(9):2182-2193
- CountryChina
- Language:English
- Abstract: ObjectiveTo investigate the effect of mucin 1 (MUC1) on the proliferation and apoptosis of nasopharyngeal carcinoma (NPC) and its regulatory mechanism. MethodsThe 60 NPC and paired para-cancer normal tissues were collected from October 2020 to July 2021 in Quanzhou First Hospital. The expression of MUC1 was measured by real-time quantitative PCR (qPCR) in the patients with PNC. The 5-8F and HNE1 cells were transfected with siRNA control (si-control) or siRNA targeting MUC1 (si-MUC1). Cell proliferation was analyzed by cell counting kit-8 and colony formation assay, and apoptosis was analyzed by flow cytometry analysis in the 5-8F and HNE1 cells. The qPCR and ELISA were executed to analyze the levels of TNF-α and IL-6. Western blot was performed to measure the expression of MUC1, NF-кB and apoptosis-related proteins (Bax and Bcl-2). ResultsThe expression of MUC1 was up-regulated in the NPC tissues, and NPC patients with the high MUC1 expression were inclined to EBV infection, growth and metastasis of NPC. Loss of MUC1 restrained malignant features, including the proliferation and apoptosis, downregulated the expression of p-IкB、p-P65 and Bcl-2 and upregulated the expression of Bax in the NPC cells. ConclusionDownregulation of MUC1 restrained biological characteristics of malignancy, including cell proliferation and apoptosis, by inactivating NF-κB signaling pathway in NPC.