Alpha-linolenic acid inhibits hepatocellular carcinoma cell growth through Farnesoid X receptor/β-catenin signaling pathway

Background Altered lipid profiles are frequently present in cancer, and it is necessary to elucidate the role of changed lipid profiles in hepatocellular carcinoma (HCC). We conducted this study to investigate the changed lipid profile in HCC tissues and discover some remarkably changed lipid compon...

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Veröffentlicht in:Nutrition & metabolism 2022-08, Vol.19 (1), p.1-57, Article 57
Hauptverfasser: Feng, Shu, Xie, Xingming, Chen, Chaochun, Zuo, Shi, Zhao, Xueke, Li, Haiyang
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Sprache:eng
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Zusammenfassung:Background Altered lipid profiles are frequently present in cancer, and it is necessary to elucidate the role of changed lipid profiles in hepatocellular carcinoma (HCC). We conducted this study to investigate the changed lipid profile in HCC tissues and discover some remarkably changed lipid components, and to explore the function of changed lipid components in HCC development. Methods Gas chromatography/mass spectrometer (GC/MS analysis) was employed to measure the abundance of fatty acids between HCC tissues and adjacent noncancerous tissues. The proliferative ability of HCC cells was determined by Cell Counting Kit-8 and EdU assays. Transwell and wound healing assays were employed to determine the migratory ability of HCC cells. Protein expression was assessed by western blot assay. Results GC/MS analysis revealed that alpha-linolenic acid was present at lower levels in HCC tissues than that in the adjacent noncancerous tissues. Alpha-linolenic acid inhibited the proliferation, migration and invasion of HCC cells in vitro. Western blotting showed that alpha-linolenic acid treatment increased Farnesoid X receptor expression and decreased β-catenin and cyclinD1 expression. Conclusions Alpha-linolenic acid suppresses HCC progression through the FXR/Wnt/β-catenin signaling pathway. Rational use of alpha-linolenic acid may prevent the occurrence of liver cancer in the future.
ISSN:1743-7075
1743-7075
DOI:10.1186/s12986-022-00693-1