Glucose uptake in the human gastric cancer cell line, MKN28, is increased by insulin stimulation

The expression of the insulin-responsive glucose transporter (GLUT) 4 was studied in three histologically different human gastric cancer cell lines, MKN28, MKN45, and STSA. RT-PCR demonstrated GLUT1 and GLUT4 mRNA in all three cell lines. MKN28 cells expressed GLUT4 protein more than MKN45 and STSA...

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Bibliographic Details
Published in:Cancer letters 1999-06, Vol.140 (1), p.69-74
Main Authors: Noguchi, Yoshikazu, Sato, Shinobu, Marat, Doulet, Doi, Chiharu, Yoshikawa, Takaki, Saito, Aya, Ito, Takaaki, Tsuburaya, Akira, Yanuma, Shunsuke
Format: Article
Language:English
Subjects:
Biological and medical sciences
Biological Transport - drug effects
Deoxyglucose - pharmacokinetics
Gastroenterology. Liver. Pancreas. Abdomen
Glucose - metabolism
Glucose Transporter Type 1
Glucose Transporter Type 4
GLUT4
Humans
Immunohistochemistry
Insulin - pharmacology
Insulin response
Medical sciences
MKN28
MKN45
Monosaccharide Transport Proteins - metabolism
Muscle Proteins
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - metabolism
Stomach Neoplasms - metabolism
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
STSA
Tumor Cells, Cultured
Tumors
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Summary:The expression of the insulin-responsive glucose transporter (GLUT) 4 was studied in three histologically different human gastric cancer cell lines, MKN28, MKN45, and STSA. RT-PCR demonstrated GLUT1 and GLUT4 mRNA in all three cell lines. MKN28 cells expressed GLUT4 protein more than MKN45 and STSA cells by immunohistochemistry. Insulin stimulation of MKN28 cells resulted in a 22% increase in glucose uptake over that found under basal conditions (0.60±0.05 fmol/cell per min after insulin stimulation versus 0.53±0.07 fmol/cell per 3 min at basal). No increase in glucose uptake occurred with insulin stimulation in MKN45 or STSA cells. We conclude that the insulin responsive GLUT4 is expressed in MKN28, MKN45, and STKM1 human gastric cancer cell lines, albeit in different amounts. The greater expression of this transporter in MKN28 cells is likely responsible for the cell's ability to increase glucose uptake with insulin stimulation. However, the role played by GLUT4 in regulating the amount of glucose uptake would not be large in those human gastric cancer cell lines.
ISSN:0304-3835
1872-7980
DOI:10.1016/S0304-3835(99)00054-3