Open Access
ARTICLE
HMGB1 promotes the proliferation and invasion of oral squamous cell carcinoma via activating epithelial-mesenchymal transformation
Jie REN1, Qian LIANG2
1
Department of Stomatology, The Sixth Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
2
The Stomatology Hospital of Guangzhou Medical University, Guangzhou, China
* Address correspondence to: Jie Ren,
BIOCELL 2019, 43(3), 199-206. https://doi.org/ 10.32604/biocell.2019.07128
Abstract
This study aimed to investigate the role of high mobility group box-1 (HMGB1) expression in oral squamous
cell carcinoma; HMGB1 promoted the proliferation and invasion of oral squamous cell carcinoma via activating
epithelial-mesenchymal transformation (EMT). In this study, RNA transfection was used to silence the expression of
HMGB1 in oral squamous cell carcinoma cells. CCK-8, cell clone formation and trans-well assays were used to detect
the proliferation and invasion of cells before and after HMGB1 silencing. qRT-PCR and Western blot were used to
detect changes in EMT marker protein expression before and after transfection. HMGB1 was significantly higher in
OSCC tissues than in adjacent tissues, and of the cell lines examined, HMGB1 was highest in SCC-9 cells. Additionally,
HMGB1 silencing decreased SCC-9 cell proliferation and viability. Down-regulation of HMBG1 expression inhibited
not only the proliferation but also the invasion of SCC-9 cells. The expression of N-cadherin, Snail, and Slug, but not
E-cadherin, were promoted after silencing HMGB1. The expression of HMGB1 in OSCC tissue and cell lines was
higher, and HMGB1 silencing decreased SCC-9 cell proliferation and invasion, suggesting that HMGB1 has positive
effects on OSCC development. Down-regulation of HMBG1 expression regulates EMT markers, suggesting that
HMBG1 promotes OSCC cell proliferation and invasion is likely to be associated with EMT activation.
Keywords
Cite This Article
REN, J., LIANG, Q. (2019). HMGB1 promotes the proliferation and invasion of oral squamous cell carcinoma via activating epithelial-mesenchymal transformation.
BIOCELL, 43(3), 199–206. https://doi.org/ 10.32604/biocell.2019.07128