FXYD6: a novel therapeutic target toward hepatocellular carcinoma
| Autor: | Hongxia Duan, Xiongfei Chen, Dongling Yang, Zhaoqing Wang, Ningxin Zhou, Xiyun Yan, Lina Song, Jing Feng, Qian Gao |
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| Rok vydání: | 2014 |
| Předmět: |
Src-ERK signaling pathway
medicine.medical_specialty Carcinoma Hepatocellular ATPase Regulator Mice Nude tumor progression Antineoplastic Agents Biochemistry Ion Channels hepatocellular carcinoma (HCC) Cell Movement Cell Line Tumor Internal medicine Drug Discovery Carcinoma Animals Humans Medicine Na+/K+-ATPase neoplasms Cell Proliferation FXYD6 Mice Inbred BALB C biology business.industry Liver Neoplasms therapeutic target Antibodies Monoclonal Cell Biology medicine.disease Xenograft Model Antitumor Assays digestive system diseases Tumor Burden HEK293 Cells Endocrinology Tumor progression Hepatocellular carcinoma Cancer research biology.protein Female Sodium-Potassium-Exchanging ATPase Signal transduction Stem cell business Research Article Biotechnology |
| Zdroj: | Protein & Cell |
| ISSN: | 1674-8018 1674-800X |
| DOI: | 10.1007/s13238-014-0045-0 |
| Popis: | FXYD6, FXYD domain containing ion transport regulator 6, has been reported to affect the activity of Na+/K+-ATPase and be associated with mental diseases. Here, we demonstrate that FXYD6 is up-regulated in hepatocellular carcinoma (HCC) and enhances the migration and proliferation of HCC cells. Up-regulation of FXYD6 not only positively correlates with the increase of Na+/K+-ATPase but also coordinates with the activation of its downstream Src-ERK signaling pathway. More importantly, blocking FXYD6 by its functional antibody significantly inhibits the growth potential of the xenografted HCC tumors in mice, indicating that FXYD6 represents a potential therapeutic target toward HCC. Altogether, our results establish a critical role of FXYD6 in HCC progression and suggest that the therapy targeting FXYD6 can benefit the clinical treatment toward HCC patients. Electronic supplementary material The online version of this article (doi:10.1007/s13238-014-0045-0) contains supplementary material, which is available to authorized users. |
| Databáze: | OpenAIRE |
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