TY - JOUR
T1 - IGF-I receptor gene activation enhanced the expression of monocarboxylic acid transporter 1 in hepatocarcinoma cells
AU - Kang, Keon Wook
AU - Jin, Ming Ji
AU - Han, Hyo Kyung
PY - 2006/4/21
Y1 - 2006/4/21
N2 - The present study aims to investigate the effect of IGF-I receptor (IGF-IR) gene activation on the expression of monocarboxylic acid transporters (MCTs) in hepatocarcinoma cells. In order to reflect malignant hepatoma, H4IIE cells (a rat hepatoma cell line) stably expressing IGF-IR (IGF-IR-H4IIE cells) have been established by retroviral infection and then the effect of IGF-IR gene up-regulation on the modulation of MCT expression was determined in IGF-IR-H4IIE cells. Immunoblot assay indicated that the expression level of MCT1 was 3.3-fold higher in IGF-IR-H4IIE cells compared to that in control cells, implying that IGF-IR signaling is coupled with the process of MCT1 expression. In contrast, the expression level of MCT2 was not affected by the IGF-IR activation, suggesting that MCT1 and MCT2 are regulated by the distinct type of signals. Furthermore, the cellular uptake of benzoic acid, a representative substrate of MCT1, was significantly (p < 0.05) enhanced following the activation of IGF-IR via the pre-incubation with IGF-I (10 ng/ml). In conclusion, MCT1 expression was up-regulated in hepatocarcinoma cells and the IGF-IR signaling appeared to be coupled with the modulation of MCT1 expression.
AB - The present study aims to investigate the effect of IGF-I receptor (IGF-IR) gene activation on the expression of monocarboxylic acid transporters (MCTs) in hepatocarcinoma cells. In order to reflect malignant hepatoma, H4IIE cells (a rat hepatoma cell line) stably expressing IGF-IR (IGF-IR-H4IIE cells) have been established by retroviral infection and then the effect of IGF-IR gene up-regulation on the modulation of MCT expression was determined in IGF-IR-H4IIE cells. Immunoblot assay indicated that the expression level of MCT1 was 3.3-fold higher in IGF-IR-H4IIE cells compared to that in control cells, implying that IGF-IR signaling is coupled with the process of MCT1 expression. In contrast, the expression level of MCT2 was not affected by the IGF-IR activation, suggesting that MCT1 and MCT2 are regulated by the distinct type of signals. Furthermore, the cellular uptake of benzoic acid, a representative substrate of MCT1, was significantly (p < 0.05) enhanced following the activation of IGF-IR via the pre-incubation with IGF-I (10 ng/ml). In conclusion, MCT1 expression was up-regulated in hepatocarcinoma cells and the IGF-IR signaling appeared to be coupled with the modulation of MCT1 expression.
KW - Benzoic acid
KW - Hepatocarcinoma cells
KW - IGF-I receptor
KW - Monocarboxylic acid transporter 1
KW - Monocarboxylic acid transporter 2
UR - http://www.scopus.com/inward/record.url?scp=33644882249&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2006.02.098
DO - 10.1016/j.bbrc.2006.02.098
M3 - Article
C2 - 16516162
AN - SCOPUS:33644882249
SN - 0006-291X
VL - 342
SP - 1352
EP - 1355
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 4
ER -