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Advanced glycation end product (AGE)-induced proliferation of HEL cells via receptor for AGE-related signal pathways
- Authors
- Kim, Ju Young; Park, Hyun Ki; Yoon, Jin Sun; Kim, Seo Ju; Kim, Eun Shil; Ahn, Kwang Sung; Kim, Dong-Sun; Yoon, Sung Soo; Kim, Byoung Kook; Lee, Young Yiul
- Issue Date
- Sep-2008
- Publisher
- Demetrios A. Spandidos Ed. & Pub.
- Keywords
- advanced glycation end product; acute myeloid leukemia; RAGE antisense S-ODN; cell proliferation; MAP kinase; apoptosis
- Citation
- International Journal of Oncology, v.33, no.3, pp 493 - 501
- Pages
- 9
- Indexed
- SCIE
SCOPUS
- Journal Title
- International Journal of Oncology
- Volume
- 33
- Number
- 3
- Start Page
- 493
- End Page
- 501
- ISSN
- 1019-6439
1791-2423
- Abstract
- 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.
- Appears in
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