LSM6 promotes cell proliferation and migration regulated by HMGB1 in laryngeal squamous cell carcinoma

Abstract

Elevated levels of high mobility group protein B1 (HMGB1) play a significant role in the pathogenesis of many diseases, but is particularly important for the formation of malignant tumors. Nonetheless, the function of HMGB1 and the underlying mechanism of laryngeal squamous cell carcinoma (LSCC) remain incompletely understood, causing uncertainty. Here we found immunohistochemistry from 97 LSCC tissues showed HMGB1 was upregulated, which was associated with poor differentiation. HMGB1 knockdown could significantly inhibit wound closure and colony formation. The full-genome gene expression microarray was performed to investigate the mechanism. After knockdown of HMGB1 by siRNA, among the expressed differential genes, 10 genes were randomly selected for validation. Then, shRNA lentivirus targeting these genes were constructed to explore their role in LSCC by cell proliferation assay. LSM6 downregulation was dramatically promoted by HMGB1 knockdown, resulting in higher expression in LSCC tissues. Furthermore, downregulation of LSM6 could significantly suppress cell proliferation, migration and colony formation. This study indicated that HMGB1 promoted LSCC cell malignant phenotypes through regulation of LSM6. We anticipate that HMGB1-LSM6 could be a putative therapeutic target for LSCC.