Human β-defensin-3 and nuclear factor-kappa B p65 synergistically promote the cell proliferation and invasion of oral squamous cell carcinoma

Yongxiu Du; Yanlan Yang; Wenbo Zhang; Chenxi Yang; Pu Xu

doi:10.1016/j.tranon.2022.101582

Human β-defensin-3 and nuclear factor-kappa B p65 synergistically promote the cell proliferation and invasion of oral squamous cell carcinoma

Transl Oncol. 2023 Jan:27:101582. doi: 10.1016/j.tranon.2022.101582. Epub 2022 Nov 18.

Authors

Yongxiu Du¹, Yanlan Yang², Wenbo Zhang², Chenxi Yang¹, Pu Xu³

Affiliations

¹ Department of Oral Mucosa Diseases, The Affiliated Haikou Hospital of Xiangya Medical College of Central South University, Hunan, China.
² Periodontics Department, The Affiliated Haikou Hospital of Xiangya Medical College of Central South University, Hunan, China.
³ General Dentistry Department, The Affiliated Haikou Hospital of Xiangya Medical College of Central South University, No. 43 Meilan Avenue, Haikou, Hunan 570208, China. Electronic address: hnxupu@163.com.

Abstract

Oral squamous cell carcinoma (OSCC) is a usual oral cancer. Therefore, it's essential to identify targets for its early diagnosis and therapy. This research aimed to explore the roles of human β-defensin-3 (hBD-3) and nuclear factor-kappa B (NF-κB) p65 in the pathogenesis and progression of OSCC. The connection between NF-κB p65 and the carcinogenesis of oral cancer was analyzed by immunohistochemical staining. The relative expressions of hBD-3 and NF-κB p65 in OSCC cells were evaluated by qRT-PCR and Western blot. Afterward, hBD-3 was knocked down, and NF-κB p65 was overexpressed. The cell viability and invasion were tested via CCK-8 and Transwell experiment, and the expression of hBD-3, NF-κB p65, and its downstream molecules was evaluated by Western blot. The expression of NF-κB p65 was increased with the aggravation of the oral submucosal fibrosis. HBD-3 and NF-κB p65 were high-expressed in OSCC cells. The viability and invasion abilities of OSCC cells that knocked down hBD-3 were markedly decreased, while they were restored by the overexpression of NF-κB p65. The expressions of NF-κB p65 and c-myc were diminished while IκB and p21 were raised with the knockdown of hBD-3. After overexpression of NF-κB p65, the expression of hBD-3 and IκB did not change markedly, while c-myc was increased and p21 was decreased dramatically. HBD-3 and NF-κB p65 facilitate the proliferation and invasion of OSCC cells, and hBD-3 may promote this process by governing the expression of NF-κB p65 and its downstream c-myc and p21.

Keywords: Carcinogenesis; Human β-defensin-3; Nuclear factor-kappa B p65; Oral squamous cell carcinoma.