Sodium taurocholate cotransporting polypeptide mediates dual actions of deoxycholic acid in human hepatocellular carcinoma cells: enhanced apoptosis versus growth stimulation

J Cancer Res Clin Oncol. 2014 Jan;140(1):133-44. doi: 10.1007/s00432-013-1554-6. Epub 2013 Nov 27.

Abstract

Purpose: The hydrophobic bile acid, deoxycholic acid (DC), can induce apoptosis in hepatocytes. The roles of DC and its transporter are not yet established in hepatocellular carcinoma (HCC) cells. We investigated DC-induced alterations in HCC cell growth, with a particular focus on the effect of the expression of bile acid (BA)-transporting Na(+)-dependent taurocholic cotransporting polypeptides (NTCPs).

Methods: We determined NTCP expression in four human HCC cell lines: Huh-BAT, Huh-7, SNU-761, and SNU-475. NTCP expression and apoptotic signaling cascades were examined by immunoblot analyses. Cell viability was assessed using the 3,4-(5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt assay. Wound healing and invasion assays were performed to evaluate cell migration and invasion abilities. Real-time polymerase chain reaction was performed to measure IL-8 expression levels. Nuclear factor kappa B (NF-κB) activity was evaluated by enzyme-linked immunosorbent assay.

Results: The HCC cell lines revealed varying NTCP expression levels, and DC treatment had dual effects, depending on NTCP expression. DC induced apoptosis in NTCP-positive HCC cells, especially under hypoxic conditions. In NTCP-negative HCC cells, simultaneous treatment with DC and cyclooxygenase inhibitor markedly decreased aggressive cellular behaviors via the inhibition of NF-κB/COX-2/IL-8 pathways.

Conclusion: Hydrophobic bile acid offers therapeutic potential for patients with advanced HCC via different mechanisms depending on NTCP expression levels within the tumor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Carcinoma, Hepatocellular / drug therapy*
  • Carcinoma, Hepatocellular / metabolism*
  • Carcinoma, Hepatocellular / pathology
  • Cell Growth Processes / drug effects
  • Cell Growth Processes / physiology
  • Cell Hypoxia / physiology
  • Cell Line, Tumor
  • Cyclooxygenase 2 / biosynthesis
  • Deoxycholic Acid / pharmacology*
  • Endoplasmic Reticulum Stress / drug effects
  • Endoplasmic Reticulum Stress / physiology
  • Enzyme Induction / drug effects
  • ErbB Receptors / antagonists & inhibitors
  • ErbB Receptors / metabolism
  • Humans
  • Interleukin-8 / biosynthesis
  • Liver Neoplasms / drug therapy*
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / pathology
  • NF-kappa B / metabolism
  • Organic Anion Transporters, Sodium-Dependent / biosynthesis*
  • Organic Anion Transporters, Sodium-Dependent / genetics
  • Organic Anion Transporters, Sodium-Dependent / metabolism
  • RNA, Small Interfering / administration & dosage
  • RNA, Small Interfering / genetics
  • Receptors, G-Protein-Coupled / antagonists & inhibitors
  • Receptors, G-Protein-Coupled / metabolism
  • Symporters / biosynthesis*
  • Symporters / genetics
  • Symporters / metabolism
  • Transfection

Substances

  • GPBAR1 protein, human
  • Interleukin-8
  • NF-kappa B
  • Organic Anion Transporters, Sodium-Dependent
  • RNA, Small Interfering
  • Receptors, G-Protein-Coupled
  • Symporters
  • Deoxycholic Acid
  • sodium-bile acid cotransporter
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • ErbB Receptors