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Amentoflavone Suppresses Cell Growth and Invasion in Renal Carcinoma Cells by Activating PPARγ

Kun Fan1,2, Xiaofu Qiu2, Yu Fu2, Kangjian Lin, Huanhui Li2, Guosheng Yang *,1,2
The third clinical medical school of Southern Medical University, Guangzhou, China, 510515.
Department of Urology, Southern Medical University Affiliated Guangdong Second Provincial General Hospital, Guangzhou 510317, China.
Corresponding Author: Yang Guosheng
Department of Urology, Guangdong Second Provincial General Hospital, Guangzhou 510317, China.
Address: 466# Xingang Middle Road, Haizhu District, Guangzhou, 510317, China.
Email: b25yfk@126.net.

Molecular & Cellular Biomechanics 2017, 14(1), 33-45. https://doi.org/10.3970/mcb.2017.014.035

Abstract

This study intends to investigate the role of amentoflavone(AF) in human clear-cell renal cell carcinoma (ccRCC) and to elucidate underlying molecular mechanisms. Materials and Methods: Human RCC cell lines Caki-1 and 786-O were used in this study. Cell proliferation, apoptosis, cell cycle distribution and invasion assays were conducted to analyze the effect of AF against ccRCC in vitro. Xenograft model and pulmonary metastasis animal model were established to evaluate the vivo therapeutic efficacy and against pulmonary metastasis ability of AF, respectively. Results: Our findings revealed that AF selectively suppressed tumor cell proliferation in a dose- and time-dependent manner. Treatment with AF significantly elevated the percent proportion of apoptotic cells and blocked cell cycle progression. Moreover, AF inhibited cell invasion in a dose-dependent fashion. Our findings revealed AF activated PPARγ, which accounts for its anti-tumor activities. Conclusions: Our findings suggest AF suppresses tumor growth and metastasis by activating PPARγ.

Keywords

PPARγ, ccRCC, amentoflavone.

Cite This Article

Fan, K., Qiu, X., Fu, Y., Lin,, K., Yang, G. (2017). Amentoflavone Suppresses Cell Growth and Invasion in Renal Carcinoma Cells by Activating PPARγ. Molecular & Cellular Biomechanics, 14(1), 33–45.



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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