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Knockdown of TACC3 Inhibits the Proliferation and Invasion of Human Renal Cell Carcinoma Cells

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Department of Urology, The Central Hospital of Wuhan, Wuhan, P.R. China

Oncology Research 2018, 26(2), 183-189. https://doi.org/10.3727/096504017X14837020772250

Abstract

Transforming acidic coiled-coil protein 3 (TACC3) is a member of the TACC family and plays an important role in regulating cell mitosis, transcription, and tumorigenesis. However, the expression pattern and roles of TACC3 in renal cell carcinoma (RCC) remain unclear. The aim of this study was to investigate the role of TACC3 in RCC. We demonstrated overexpression of TACC3 in human RCC cell lines at both RNA and protein levels. Moreover, knockdown of TACC3 repressed RCC cell proliferation, migration, and invasion in vitro. In addition, knockdown of TACC3 inactivated PI3K/Akt signaling in RCC cells. Furthermore, knockdown of TACC3 significantly reduced tumor growth in xenograft tumor-bearing mice. Taken together, our findings showed that TACC3 was increased in human RCC cell lines, and knockdown of TACC3 inhibited the ability of cell proliferation, migration, invasion, and tumorigenesis in vivo. Therefore, TACC3 may act as a therapeutic target for the treatment of human RCC.

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APA Style
Guo, F., Liu, Y. (2018). Knockdown of TACC3 inhibits the proliferation and invasion of human renal cell carcinoma cells. Oncology Research, 26(2), 183-189. https://doi.org/10.3727/096504017X14837020772250
Vancouver Style
Guo F, Liu Y. Knockdown of TACC3 inhibits the proliferation and invasion of human renal cell carcinoma cells. Oncol Res. 2018;26(2):183-189 https://doi.org/10.3727/096504017X14837020772250
IEEE Style
F. Guo and Y. Liu, “Knockdown of TACC3 Inhibits the Proliferation and Invasion of Human Renal Cell Carcinoma Cells,” Oncol. Res., vol. 26, no. 2, pp. 183-189, 2018. https://doi.org/10.3727/096504017X14837020772250



cc Copyright © 2018 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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