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.
Highlights
Liver cancer is a serious disease with poor prognosis [1]
One of the major products of glycolysis, pyruvate, is converted to citrate in the mitochondria as part of the TCA cycle; citrate is exported to the cytosol by the citrate carrier SLC25A1 where its cleavage by the enzyme ATP citrate lyase provides substrates for lipid biosynthesis [7]
Cells can import citrate from the blood stream, where its concentrations greatly exceed those in the mitochondria, via SLC13A5, which is highly expressed in liver cells [9]
Summary
Liver cancer is a serious disease with poor prognosis [1]. Similar to other cancers, liver cancer cells exhibit altered energy balance, including changes in lipid metabolism as well as the glycolytic pathway and TCA2 cycle. Given the central role of citrate for multiple metabolic pathways, previous studies have focused primarily on SLC25A1 as a possible target to modulate human health [8]. Cells can import citrate from the blood stream, where its concentrations greatly exceed those in the mitochondria, via SLC13A5, which is highly expressed in liver cells [9].
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