Hongjun Xie1, Shengyun Huang1, Wengang Li1, Hongbo Zhao1, Tianqi Zhang1, Dongsheng Zhang2. 1. Department of Oral & Maxillofacial Surgery, Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China. 2. Department of Oral & Maxillofacial Surgery, Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China. Electronic address: ds63zhang@sdu.edu.cn.
Abstract
OBJECTIVE: This study investigated the clinical significance of Shp2 protein expression in oral squamous cell carcinoma (OSCC) and elucidated its biologic significance in OSCC cells. STUDY DESIGN: A total of 88 OSCC cases were used to assess Shp2 expression, out of which 70 were for immunohistochemistry and 18 paired tumors vs normal tissues were for Western blot of Shp2 expression. OSCC cells were used to assess the effects of Shp2 knockdown for cell viability, apoptosis, invasion, and protein expressions. RESULTS: Expression of Shp2 protein was significantly upregulated in OSCC tissues compared with the normal tissues, and Shp2 overexpression was associated with advanced tumor clinical stages and lymph node metastasis ex vivo. Knockdown of Shp2 expression in vitro inhibited OSCC cell viability and invasion but induced apoptosis by regulating expression of the apoptosis-related proteins. CONCLUSIONS: The data indicated that Shp2 may play an important role in OSCC progression. Further studies will investigate whether a target of Shp2 expression could be a novel therapeutic strategy for clinical control of OSCC.
OBJECTIVE: This study investigated the clinical significance of Shp2 protein expression in oral squamous cell carcinoma (OSCC) and elucidated its biologic significance in OSCC cells. STUDY DESIGN: A total of 88 OSCC cases were used to assess Shp2 expression, out of which 70 were for immunohistochemistry and 18 paired tumors vs normal tissues were for Western blot of Shp2 expression. OSCC cells were used to assess the effects of Shp2 knockdown for cell viability, apoptosis, invasion, and protein expressions. RESULTS: Expression of Shp2 protein was significantly upregulated in OSCC tissues compared with the normal tissues, and Shp2 overexpression was associated with advanced tumor clinical stages and lymph node metastasis ex vivo. Knockdown of Shp2 expression in vitro inhibited OSCC cell viability and invasion but induced apoptosis by regulating expression of the apoptosis-related proteins. CONCLUSIONS: The data indicated that Shp2 may play an important role in OSCC progression. Further studies will investigate whether a target of Shp2 expression could be a novel therapeutic strategy for clinical control of OSCC.