Flipping a citrate switch on liver cancer cells

J Biol Chem. 2017 Aug 18;292(33):13902-13903. doi: 10.1074/jbc.H117.783860.

Abstract

Energy homeostasis and oncogenic signaling are critical determinants of the growth of human liver cancer cells, providing a strong rationale to elucidate the regulatory mechanisms for these systems. A new study reports that loss of solute carrier family 13 member 5, which transports citrate across cell membranes, halts liver cancer cell growth by altering both energy production and mammalian target of rapamycin signaling in human liver cancer cell lines and in both an in vitro and in vivo model of liver tumors, suggesting a new target for liver cancer chemoprevention and/or chemotherapy.

Publication types

  • Review
  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Citric Acid Cycle*
  • Energy Metabolism
  • Hepatoblastoma / metabolism
  • Hepatoblastoma / pathology
  • Hepatoblastoma / therapy*
  • Humans
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / pathology
  • Liver Neoplasms / therapy*
  • Mice, Nude
  • Neoplasm Proteins / antagonists & inhibitors*
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism
  • RNAi Therapeutics*
  • Symporters / antagonists & inhibitors*
  • Symporters / genetics
  • Symporters / metabolism
  • Tumor Burden
  • Xenograft Model Antitumor Assays

Substances

  • Neoplasm Proteins
  • SLC13A5 protein, human
  • Symporters