scholarly journals Over-expression of protein tyrosine phosphatase 4A2 correlates with tumor progression and poor prognosis in nasopharyngeal carcinoma

Oncotarget ◽  
2017 ◽  
Vol 8 (44) ◽  
pp. 77527-77539 ◽  
Author(s):  
Ying Gao ◽  
Mengping Zhang ◽  
Zhousan Zheng ◽  
Ying He ◽  
Yujia Zhu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Tumor Progression ◽  
Protein Tyrosine Phosphatase ◽  
Poor Prognosis ◽  
Tyrosine Phosphatase ◽  
Protein Tyrosine ◽  
Over Expression

scholarly journals Functional Analysis of a Cell Cycle–Associated, Tumor-Suppressive Gene, Protein Tyrosine Phosphatase Receptor Type G, in Nasopharyngeal Carcinoma

2008 ◽  
Vol 68 (19) ◽  
pp. 8137-8145 ◽  
Author(s):  
Arthur Kwok Leung Cheung ◽  
Hong Lok Lung ◽  
Siu Chun Hung ◽  
Evan Wai Lok Law ◽  
Yue Cheng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Functional Analysis ◽  
Nasopharyngeal Carcinoma ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Receptor Type ◽  
Protein Tyrosine ◽  
A Cell

scholarly journals Leptin resistance following over-expression of protein tyrosine phosphatase 1B in liver

2006 ◽  
Vol 36 (1) ◽  
pp. 163-174 ◽  
Author(s):  
N T Lam ◽  
S D Covey ◽  
J T Lewis ◽  
S Oosman ◽  
T Webber ◽  
...  
Keyword(s):  
Food Intake ◽  
Plasma Glucose ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Leptin Resistance ◽  
Protein Tyrosine Phosphatase 1B ◽  
High Fat ◽  
Peripheral Tissues ◽  
Protein Tyrosine ◽  
Over Expression

Obesity is typically associated with resistance to leptin, yet the mechanism by which leptin signaling becomes impaired is poorly understood. Here we sought to determine if the development of obesity and leptin resistance correlates with increased expression of protein tyrosine phosphatase 1B (PTP1B) in peripheral tissues and whether over-expression of this phosphatase, specifically in liver, could alter the leptin-mediated effects on feeding and glucose metabolism. Obesity was induced in mice through a high-fat diet that resulted in hyperglycemia, hyperinsulinemia and hyperleptinemia. Resistance to leptin was confirmed as exogenous leptin administration reduced food intake in animals on low-fat, but not high-fat diets. Diet-induced resistance to leptin and insulin was associated with increased hepatic levels of PTP1B. Intriguingly, hepatic adenoviral over-expression of PTP1B in ob/ob mice attenuated the ability of exogenous leptin to reduce both plasma glucose levels and food intake. These findings suggest that leptin reduces both plasma glucose and food intake in part through actions on the liver, and hepatic leptin resistance resulting from over-expression of PTP1B may contribute to the development of both diabetes and obesity.

scholarly journals Protein tyrosine phosphatase receptor type D gene promotes radiosensitivity via STAT3 dephosphorylation in nasopharyngeal carcinoma

Oncogene ◽  
2021 ◽  
Author(s):  
Yanling Lin ◽  
Xiaohan Zhou ◽  
Kaifan Yang ◽  
Yuting Chen ◽  
Lingzhi Wang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Protein Tyrosine Phosphatase ◽  
Molecular Mechanisms ◽  
Tyrosine Phosphatase ◽  
Receptor Type ◽  
Therapeutic Modality ◽  
Protein Tyrosine ◽  
Type D ◽  
Radiation Induced

AbstractRadiotherapy is essential to the treatment of nasopharyngeal carcinoma (NPC) and acquired or innate resistance to this therapeutic modality is a major clinical problem. However, the underlying molecular mechanisms in the radiation resistance in NPC are not fully understood. Here, we reanalyzed the microarray data from public databases and identified the protein tyrosine phosphatase receptor type D (PTPRD) as a candidate gene. We found that PTPRD was downregulated in clinical NPC tissues and NPC cell lines with its promoter hypermethylated. Functional assays revealed that PTPRD overexpression sensitized NPC to radiation in vitro and in vivo. Importantly, miR-454-3p directly targets PTPRD to inhibit its expression and biological effect. Interestingly, mechanistic analyses indicate that PTPRD directly dephosphorylates STAT3 to enhance Autophagy-Related 5 (ATG5) transcription, resulting in triggering radiation-induced autophagy. The immunohistochemical staining of 107 NPC revealed that low PTPRD and high p-STAT3 levels predicted poor clinical outcome. Overall, we showed that PTPRD promotes radiosensitivity by triggering radiation-induced autophagy via the dephosphorylation of STAT3, thus providing a potentially useful predictive biomarker for NPC radiosensitivity and drug target for NPC radiosensitization.

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