β‐Ionone represses renal cell carcinoma progression through activating LKB1/AMPK‐triggered autophagy

Author:

Hou Tao123ORCID,Wang Yuzhao123,Dan Weichao123,Wei Yi123,Liu Bo123,Que Taotao123,Lei Yuzeshi123ORCID,Yu Bixin1,Zeng Jin123,Fan Yizeng123,Li Lei123

Affiliation:

1. Department of Urology The First Affiliated Hospital of Xi'an Jiaotong University Xi'an Shaanxi China

2. Key Laboratory of Environment and Genes Related to Diseases Ministry of Education Xi'an Shaanxi China

3. Key Laboratory for Tumor Precision Medicine of Shaanxi Province The First Affiliated Hospital of Xi'an Jiaotong University Xi'an Shaanxi China

Abstract

Abstractβ‐Ionone, the end ring analog of β‐carotenoids, has been proven to have an antitumor effect in a variety of cancers. In this study, we investigated the impact of β‐ionone on renal cell carcinoma (RCC) cell lines (786‐O and ACHN) using colony formation assays, flow cytometry analysis, and western blot analysis. We found that β‐ionone effectively inhibited the proliferation of RCC cells in vitro, which was also confirmed in a xenograft model. Moreover, we found that β‐ionone could induce autophagy, as indicated by LC3 puncta in 786‐O and ACHN cell lines and the expression of LC3 in β‐ionone‐treated RCC cells. To further explore the underlying mechanism, we assessed liver kinase B1/AMP‐activated protein kinase (LKB1/AMPK) signaling pathway activity, and the results showed that β‐ionone inhibited the proliferation of RCC cells by inducing autophagy via the LKB1/AMPK signaling pathway. In summary, our findings provide a new therapeutic strategy of β‐ionone‐induced autophagy in RCC.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Toxicology,Molecular Biology,Molecular Medicine,Biochemistry,General Medicine

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