| ORIGINAL ARTICLE |
|
| Ahead of Print |
|
|
Knockdown of FKBP3 suppresses nasopharyngeal carcinoma cell growth, invasion and migration, deactivated NF-κB/IL-6 signaling pathway through inhibiting histone deacetylase 2 expression
Jiadi Dong, Jingjing Chen, Qun Li, Shijie Qiu
Department of Otorhinolaryngology Head and Neck Surgery, Ningbo Medical Center Li Huili Hospital, Ningbo, Zhejiang, China
Correspondence Address:
Shijie Qiu,
Department of Otorhinolaryngology Head and Neck Surgery, Ningbo Medical Center Li Huili Hospital, Ningbo, No. 57, Xingning, Yinzhou
China
 Source of Support: None, Conflict of Interest: None DOI: 10.4103/cjop.CJOP-D-22-00075
|
|
|
Nasopharyngeal carcinoma (NPC) is a prevalent malignant tumor worldwide. FKBP3 has been reported to participate in tumorigenesis. Nevertheless, the role and mechanism of FKBP3 in NPC remains unclear. In this study, FKBP3 expression was observed to upregulate in NPC patients and cells. Moreover, knockdown of FKBP3 suppressed cell growth, invasion, and migration in HK1 and C666-1 cells. Mechanically, FKBP3 could enhance the p-p65 expression and activated p65 signaling pathway and increased interleukin-6 (IL-6) expression through enhancing histone deacetylase 2 (HDAC2) expression. In rescued experiment, the overexpression of HDAC2 restored diminished cell growth, invasion, and migration caused by FKBP3 depletion. In summary, the knockdown of FKBP3 suppressed NPC cell growth, invasion and migration, deactivated nuclear factor-κB/IL-6 signaling pathway through inhibiting HDAC2 expression, providing a potential therapeutic strategy for NPC treatment.
|
|
|
|
|
|
|
Search Pubmed for