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J Biol Chem, Vol. 275, Issue 8, 5347-5354, February 25, 2000
From the Tumor associated gene-1/L amino acid
transporter-1 (TA1/LAT-1) was recently identified as a light chain of
the CD98 amino acid transporter and cellular activation marker. Our
previous studies with primary rat hepatocyte cultures demonstrated that TA1 RNA levels were responsive to media amino acid concentrations, suggesting adaptive regulation. High level TA1 expression associated with transformed cells also suggested a role in tumor progression. The
present study examined the relationship of TA1/CD98 expression, adaptive response, and associated amino acid transport to neoplastic transformation using a panel of well characterized rat hepatic cell
lines. We found 1) increased expression of TA1 in response to amino
acid depletion, specific for arginine but not glutamine; 2) loss of TA1
response to arginine in
TA1/LAT-1/CD98 Light Chain and System L Activity, but Not
4F2/CD98 Heavy Chain, Respond to Arginine Availability in Rat Hepatic
Cells
LOSS OF RESPONSE IN TUMOR CELLS*
,,,
Division of Medical Oncology and
§ Department of Surgery, Rhode Island Hospital, Brown
University School of Medicine and Graduate Program in Pathobiology,
Providence, Rhode Island 02903 and the ¶ Department of Pathology,
University of North Carolina, Chapel Hill, North Carolina 27599
-glutamyl transpeptidase-positive transformed and tumorigenic cells; 3) no appreciable response of
4F2/CD98 heavy chain to arginine levels; and 4) correlation of system L
amino acid transport activity in response to arginine with changes in
TA1/LAT-1 mRNA but not total immunoreacting protein. Our results
suggest this CD98 light chain may act as an environmental sensor,
responding to amino acid availability and that its regulation is
complex. We hypothesize that altered TA1 expression is an early event
in hepatocarcinogenesis giving neoplastic cells a growth or survival
advantage, particularly under conditions of limited amino acid availability.
*
This work was supported by NIEHS, National Institutes of
Health Training Grant T32ESO7272, National Institutes of Health Grant CA73611, and funds from the Rhode Island Hospital George Oncology Foundation.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Medical Oncology,
Rhode Island Hospital, 593 Eddy St., Providence, RI 02903. Tel.: 401-444-8860; E-mail: Nancy_Thompson@brown.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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