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  • Open Access

    ARTICLE

    Tumor Protein D52 (TPD52) Inhibits Growth and Metastasis in Renal Cell Carcinoma Cells Through the PI3K/Akt Signaling Pathway

    Zhenhua Zhao1, Hui Liu1, Junqing Hou, Tieqiang Li, Xinyi Du, Xiaolei Zhao, Wenchao Xu, Weibo Xu, Junkai Chang

    Oncology Research, Vol.25, No.5, pp. 773-779, 2017, DOI:10.3727/096504016X14774889687280

    Abstract Tumor protein D52 (TPD52) is a member of the TPD52-like protein family and plays different roles in various types of malignancies. However, its role in renal cell carcinoma (RCC) is still unclear. In this study, we investigated the role of TPD52 in RCC. The mechanism of TPD52 in RCC was also investigated. Our data demonstrated that the expression levels of TPD52 in both mRNA and protein were significantly decreased in RCC cells. Overexpression of TPD52 inhibited proliferation, migration, and invasion with decreased epithelial–mesenchymal transition (EMT) phenotype in RCC cells, as well as attenuated tumor growth More >

  • Open Access

    ARTICLE

    Downregulation of MicroRNA-449 Promotes Migration and Invasion of Breast Cancer Cells by Targeting Tumor Protein D52 (TPD52)

    Zhiling Zhang, Jiawei Wang, Runfang Gao, Xuan Yang, Yafen Zhang, Jie Li, Jing Zhang, Xingjuan Zhao, Chunfang Xi, Xiaoting Lu

    Oncology Research, Vol.25, No.5, pp. 753-761, 2017, DOI:10.3727/096504016X14772342320617

    Abstract Our study aimed to investigate whether microRNA-449 (miR-449) plays a key role in regulating the migration and invasion of breast cancer cells via targeting tumor protein D52 (TPD52). The results of the qRT-PCR and Western blotting showed that, in comparison with normal breast tissues and cells, miR-449 was significantly downregulated in breast cancer tissues and cells, while TPD52 was markedly upregulated. After transfection with an miR-449 inhibitor, suppression of miR-449 significantly promoted cell migration and invasion. Also, when miR-449 was overexpressed by transfection with miR-449 mimics, E-cadherin expression significantly increased, and the expression of N-cadherin More >

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