PT - JOURNAL ARTICLE AU - HISAO IMAI AU - KYOICHI KAIRA AU - NOBORU ORIUCHI AU - KIMIHIRO SHIMIZU AU - HIDEYUKI TOMINAGA AU - NORIKO YANAGITANI AU - NORIAKI SUNAGA AU - TAMOTSU ISHIZUKA AU - SHUSHI NAGAMORI AU - KANYARAT PROMCHAN AU - TAKASHI NAKAJIMA AU - NOBUYUKI YAMAMOTO AU - MASATOMO MORI AU - YOSHIKATSU KANAI TI - Inhibition of L-type Amino Acid Transporter 1 Has Antitumor Activity in Non-small Cell Lung Cancer DP - 2010 Dec 01 TA - Anticancer Research PG - 4819--4828 VI - 30 IP - 12 4099 - http://ar.iiarjournals.org/content/30/12/4819.short 4100 - http://ar.iiarjournals.org/content/30/12/4819.full SO - Anticancer Res2010 Dec 01; 30 AB - Background: L-type amino acid transporter 1 (LAT1) is highly expressed in various human neoplasms. Antitumor activity of inhibiting LAT1 was analyzed in non-small cell lung cancer (NSCLC). Materials and Methods: Expression of LAT1 mRNA in 54 lung cancer cell lines was examined by RT-PCR. An inhibitor of LAT1, 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH), was administered to H1395 cell. LAT1 expression was examined in correlation with clinical features and outcome in 51 NSCLC patients. Results: Inhibition of LAT1 by BCH reduced cell viability in H1395 cells. Furthermore, co-administration of gefitinib with BCH reduced the viability of the cells more than either agent alone. Inhibition of LAT1 reduced the level of phosphorylation of mTOR, p70S6K and 4EBP1. LAT1 protein expression was closely associated with wild type EGFR, and was an independent significant factor to predict a poor prognosis. Conclusion: Inhibition of LAT1 may be a new rationale to the effective therapy of NSCLC without EGFR mutation.