Research Papers:
Overexpressed tryptophanyltRNA synthetase an angiostatic protein enhances oral cancer cell invasiveness
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Chien-Wei Lee1, Kai-Ping Chang3, Yan-Yu Chen5, Ying Liang5, Chuen Hsueh4,5,6, Jau-Song Yu1,2,5, Yu-Sun Chang1,5, Chia-Jung Yu1,2,5
1Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan
2Department of Cell and Molecular Biology, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan
3Department of Otolaryngology-Head and Neck Surgery, Chang Gung Memorial Hospital, Lin-Kou, Tao-Yuan, Taiwan
4Department of Pathology, Chang Gung Memorial Hospital, Lin-Kou, Tao-Yuan, Taiwan
5Molecular Medicine Research Center, Chang Gung University, Tao-Yuan, Taiwan
6Pathology Core, Chang Gung University, Tao-Yuan, Taiwan
Correspondence to:
Chia-Jung Yu, e-mail: [email protected]
Keywords: tryptophanyl-tRNA synthetase, oral squamous cell carcinoma, migration, invasion
Received: February 10, 2015 Accepted: June 05, 2015 Published: June 17, 2015
ABSTRACT
Oral squamous cell carcinoma (OSCC) is one of the most common neoplasms worldwide. Previously, we identified the angiostatic agent tryptophanyl-tRNA synthetase (TrpRS) as a dysregulated protein in OSCC based on a proteomics approach. Herein, we show that TrpRS is overexpressed in OSCC tissues (139/146, 95.2%) compared with adjacent normal tissues and that TrpRS expression positively correlates with tumor stage, overall TNM stage, perineural invasion and tumor depth. Importantly, the TrpRS levels were significantly higher in tumor cells from metastatic lymph nodes than in corresponding primary tumor cells. TrpRS knockdown or treatment with conditioned media obtained from TrpRS-knockdown cells significantly reduced oral cancer cell viability and invasiveness. TrpRS overexpression promoted cell migration and invasion. In addition, the extracellular addition of TrpRS rescued the invasion ability of TrpRS-knockdown cells. Subcellular fractionation and immunofluorescence staining further revealed that TrpRS was distributed on the cell surface, suggesting that secreted TrpRS promotes OSCC progression via an extrinsic pathway. Collectively, our results demonstrated the clinical significance and a novel role of TrpRS in OSCC.