Lei Wu1, Lanying Gao1, Decai Kong1, Hongfeng Xue2. 1. Department of General Surgery, Heze Municipal Hospital, No 2888 Caozhou Road, Mudan District, Heze, 274000, Shandong, China. 2. Department of General Surgery, Heze Municipal Hospital, No 2888 Caozhou Road, Mudan District, Heze, 274000, Shandong, China. xuehongfeng123@sina.com.
Abstract
BACKGROUND: The protein tyrosine phosphatase delta (PTPRD) is a tumor suppressor, and its role in gastric cancer (GC) remains poorly understood. METHODS: The expressions of PTPRD were determined based on public data. In addition, the mRNA expressions of PTPRD in the GC samples, and the expressions of PTPRD in the GC cell lines including HGC27, SGC790, and BGC823, and gastric epithelial cell line GES-1 were determined by western blotting and quantitative real-time PCR. Furthermore, PTPRD siRNA was transfected into the HGC27 cell line, and then, cell proliferation, migration, and invasion were evaluated. The activity of signal transducer and activator of transcription 3 (STAT3) pathways in HGC27 cells transfected with PTPRD siRNA was determined by western blotting. RESULTS: PTPRD deletion was found in the GC patients, and this deletion was found to be correlated with poor prognosis in the GC patients. Expression of PTPRD was significantly downregulated in gastric carcinoma specimens and tumor cell lines when compared with those in normal controls. PTPRD also plays a key role in the GC cells proliferation, invasion, and migration. Silencing PTPRD expression by siRNA dramatically promoted GC cells proliferation, invasion, and migration. Mechanism study demonstrated that phosphorylation of STAT3 was inhibited by silencing PTPRD expression and the according changes including inhibition of cell migration and invasion were observed. CONCLUSION: This study supports PTPRD as a tumor suppressor and could be served as a marker for prognostic of GC. Silencing PTPRD could be a potential therapeutic in GC.
BACKGROUND: The protein tyrosine phosphatase delta (PTPRD) is a tumor suppressor, and its role in gastric cancer (GC) remains poorly understood. METHODS: The expressions of PTPRD were determined based on public data. In addition, the mRNA expressions of PTPRD in the GC samples, and the expressions of PTPRD in the GC cell lines including HGC27, SGC790, and BGC823, and gastric epithelial cell line GES-1 were determined by western blotting and quantitative real-time PCR. Furthermore, PTPRD siRNA was transfected into the HGC27 cell line, and then, cell proliferation, migration, and invasion were evaluated. The activity of signal transducer and activator of transcription 3 (STAT3) pathways in HGC27 cells transfected with PTPRD siRNA was determined by western blotting. RESULTS:PTPRD deletion was found in the GC patients, and this deletion was found to be correlated with poor prognosis in the GC patients. Expression of PTPRD was significantly downregulated in gastric carcinoma specimens and tumor cell lines when compared with those in normal controls. PTPRD also plays a key role in the GC cells proliferation, invasion, and migration. Silencing PTPRD expression by siRNA dramatically promoted GC cells proliferation, invasion, and migration. Mechanism study demonstrated that phosphorylation of STAT3 was inhibited by silencing PTPRD expression and the according changes including inhibition of cell migration and invasion were observed. CONCLUSION: This study supports PTPRD as a tumor suppressor and could be served as a marker for prognostic of GC. Silencing PTPRD could be a potential therapeutic in GC.
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