Literature DB >> 29742507

Cyanidin Curtails Renal Cell Carcinoma Tumorigenesis.

Xiaobing Liu1, Dangling Zhang1, Yaxing Hao2, Qian Liu1, Yuqi Wu1, Xin Liu1, Jing Luo1, Tao Zhou1, Bishao Sun1, Xing Luo1, Jie Xu1, Qingqing Wang1, Zhenxing Yang1, Longkun Li1.   

Abstract

BACKGROUND/AIMS: Cyanidin is an anthocyanin found in many foods. Although its variable antioxidant levels are well-documented, little is known about its effects on renal cell carcinoma (RCC) tumorigenesis. This study, therefore, investigated the effects of cyanidin on the proliferation, migration, and invasion of renal cell carcinoma lines and demonstrated, for the first time, significant inhibitory effects of cyanidin on RCC tumorigenesis.
METHODS: RCC cells were treated with different doses of cyanidin and the effects were tested by Cell Counting Kit-8 reagent, clone formation assay, transwell assay, and flow cytometry. Moreover, the cyanidin-mediated mechanism that curtailed tumorigenesis was analyzed by RNA sequencing (RNA-seq). Sequencing data from The Cancer Genome Atlas (TCGA) were used to compare the expression of both early growth response protein 1 (EGR1) and selenoprotein W (SEPW1) in RCC and tumor-free adjacent normal tissue samples. Real-time PCR (RT-PCR) and/or western blot were used to assess the expression of E-cadherin, cleaved-caspase3, Bcl2, p62, and ATG4.
RESULTS: We found significantly greater induction of cell-cycle arrest, apoptosis, and suppression of RCC cell invasion and migration at concentrations of 25 µM and 100 µM than at a concentration of 50 µM. It was also discovered, first through RNA-seq then confirmed by RT-PCR, that cyanidin (100 µM) inhibited RCC carcinogenesis through EGR1 and SEPW1. TCGA data indicated that the expression level of EGR1 was lower and that of SEPW1 was higher in RCC tumor tissue than in normal tissues. Moreover, western blot and/or RT-PCR indicated that cleaved-caspase3 was enhanced and E-cadherin was inhibited by cyanidin treatment. Furthermore, western blot and RT-PCR also showed regulation of p62 and ATG4, which are associated with autophagy. Cyanidin in vivo significantly inhibited the growth of xenografts in nude mice.
CONCLUSIONS: The results of this study showed the therapeutic potential of cyanidin for the treatment of RCC and the prevention of recurrence and metastasis.
© 2018 The Author(s). Published by S. Karger AG, Basel.

Entities:  

Keywords:  Apoptosis; Cyanidin; Invasion; Migration; Renal cell carcinoma

Mesh:

Substances:

Year:  2018        PMID: 29742507     DOI: 10.1159/000489658

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


  7 in total

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  7 in total

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