CD147 silencing inhibits tumor growth by suppressing glucose transport in melanoma
Metrics: PDF 974 views | HTML 863 views | ?
Juan Su1,2, Tianyuan Gao1,3, Minghao Jiang1,4, Lisha Wu5, Weiqi Zeng1,2, Shuang Zhao1,2, Cong Peng1,2 and Xiang Chen1,2
1 Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China
2 Hunan Key Laboratory of Skin Cancer and Psoriasis, Xiangya Hospital, Central South University, Changsha, Hunan, China
3 Department of Dermatology, the First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shanxi
4 Department of Anesthesiology, Xiangya Hospital, Central South University, Changsha, Hunan, China
5 Institute of Medical Science Research, Xiangya Hospital, Central South University, Hunan, China
Xiang Chen, email:
Cong Peng, email:
Keywords: melanoma; CD147; glycolysis; GLUT-1; PI3K/Akt pathway
Received: June 29, 2016 Accepted: August 15, 2016 Published: August 19, 2016
Melanoma is a very malignant disease and there are still no effective treatments. CD147 participates in the carcinogenesis of multiple human cancers and GLUT-1, as a glucose transporter, is associated with tumor growth. However, the function of CD147 and GLUT-1 in melanoma have not been completely understood. Thus, in this study we investigated the expression of CD147 and GLUT-1 in melanoma tissue, which were overexpressed compared with that in nevus tissue. In addition, CD147 and GLUT-1 were co-localized in the cytoplasm of human melanoma A375 cells. Immunoprecipitation proved that CD147 interacted with GLUT-1 at D105-199. Silencing CD147 by specific siRNA could downregulate GLUT-1 level via inhibiting PI3K/Akt signaling and decrease glucose uptake in A375 cells. In vivo experiments also supported that CD147 knockdown suppressed the tumor growth in melanoma subcutaneous mice model, observed by micro PET/CT. Our results could help validate CD147 as a new therapeutic target for treating melanoma.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.