Advanced glycation end product (AGE)-induced proliferation of HEL cells via receptor for AGE-related signal pathways.
This study investigated whether advanced glycation end products (AGE) and RAGE (receptor for AGE) are involved in the proliferation of leukemia cells. AGE strongly induced the proliferation of primary acute myeloid leukemia (AML) cells and cell lines. MAP kinase, PI3K and JAK/STAT pathways were involved in cellular proliferation of HEL cells by AGE. RAGE antisense S-ODN effectively inhibited cell growth, induced apoptosis and reversed AGE-induced expression of targeting molecules in HEL cells. The study demonstrated for the first time that AGE directly induced human AML cell proliferation via the MAPK, PI3K and JAK/STAT pathways.
Kim
Ju Young
JY
Cancer Research Institute, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Korea.
Park
Hyun Ki
HK
Yoon
Jin Sun
JS
Kim
Seo Ju
SJ
Kim
Eun Shil
ES
Ahn
Kwang Sung
KS
Kim
Dong-Sun
DS
Yoon
Sung Soo
SS
Kim
Byoung Kook
BK
Lee
Young Yiul
YY
D015153:Blotting, Western; D049109:Cell Proliferation; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005434:Flow Cytometry; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006801:Humans; D047468:Immunoprecipitation; D015470:Leukemia, Myeloid, Acute / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050791:STAT Transcription Factors / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D014407:Tumor Cells, Cultured
D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D050791:STAT Transcription Factors; D019869:Phosphatidylinositol 3-Kinases; D048049:Extracellular Signal-Regulated MAP Kinases