Abstract
Background Amino acids such as glutamine are important for tumor cell growth, survival and metabolism. There is renewed interest in glutamine metabolism due to the importance of reductive carboxylation in cancer. The amino acid transporter ASCT2 (SLC1A5) mediates uptake of glutamine in cancer cells. We have recently reported that ASCT2 expression is significantly upregulated in melanoma, and ASCT2 inhibition significantly decreases glutamine uptake, cell growth, cell cycle and mTORC1 pathway activation [1]. We have previously shown that ASCT2 expression is regulated by the androgen receptor in prostate cancer [2], and in this current study we further examine ASCT2 expression levels in prostate cancer. Our specific aim was to determine the impact of inhibiting ASCT2-mediated glutamine uptake and metabolism on cell growth.
Highlights
Amino acids such as glutamine are important for tumor cell growth, survival and metabolism
Inhibition of ASCT2 function by benzylserine led to decreases in glutamine uptake, glutamine metabolism, cell cycle progression, mTORC1 pathway activation and cell growth
ASCT2-mediated glutamine uptake is essential for multiple pathways including glutamine metabolism and mTORC1 signaling, thereby regulating cellular energy, protein synthesis and cell growth
Summary
Inhibition of glutamine uptake regulates mTORC1, glutamine metabolism and cell growth in prostate cancer. From Metabolism, Diet and Disease 2014: Cancer and metabolism Washington DC, USA. 28-30 May 2014
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