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Vitamin K2 suppresses proliferation and motility of hepatocellular carcinoma cells by activating steroid and xenobiotic receptor.

Abstract
Vitamin K2, known as a cofactor for gamma-carboxylase, also serves as a ligand of a nuclear receptor, Steroid and Xenobiotic Receptor (SXR). Several clinical trials revealed that vitamin K2 reduced de novo formation and recurrence of hepatocellular carcinoma (HCC). To examine the role of SXR in HCC as a receptor activated by vitamin K2, the cells stably overexpressing SXR were established using a HCC cell line, HuH7. Overexpression of SXR resulted in reduced proliferation and motility of the cells. Further suppression of proliferation and motility was observed when SXR overexpressing clones were treated with vitamin K2. These results suggest that the activation of SXR could contribute to tumor suppressive effects of vitamin K2 on HCC cells.
AuthorsKotaro Azuma, Tomohiko Urano, Yasuyoshi Ouchi, Satoshi Inoue
JournalEndocrine journal (Endocr J) Vol. 56 Issue 7 Pg. 843-9 ( 2009) ISSN: 1348-4540 [Electronic] Japan
PMID19550077 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Pregnane X Receptor
  • Receptors, Steroid
  • Vitamin K 2
  • menatetrenone
  • Rifampin
Topics
  • Carcinoma, Hepatocellular (drug therapy, pathology, physiopathology)
  • Cell Line, Tumor
  • Cell Movement (drug effects)
  • Cell Proliferation (drug effects)
  • Hep G2 Cells
  • Humans
  • Liver Neoplasms (drug therapy, pathology)
  • Pregnane X Receptor
  • Receptors, Steroid (drug effects, physiology)
  • Rifampin (pharmacology)
  • Vitamin K 2 (analogs & derivatives, pharmacology, therapeutic use)

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