Cancer Lett. 2009;274(2):259-65.
Enhanced interleukin-2 diphtheria toxin conjugate-induced growth suppression in retinoic acid-treated hypoxic hepatocellular carcinoma cells.
제1저자 김보현 · 교신저자 윤정환
소속 (1)
- Department of Internal Medicine and the Liver Research Institute, Seoul National University College of Medicine, 28 Yungun-dong, Chongno-gu, Seoul 110-744, Republic of Korea.
Abstract
Hypoxia induces survival signals in hepatocellular carcinoma (HCC). Hypoxia and retinoic acid (RA) may also induce interleukin-2 (IL-2) receptor expression, and thus we evaluated if RA and IL-2 receptor-targeted therapy are indicated in hypoxic HCCs. RA induced IL-2 receptor expression (R alpha, R beta, R gamma) in HCC cells, whereas hypoxia specifically induced IL-2 R gamma expression. IL-2 stimulated hypoxic HCC cell growth via p42/44 MAPK activation. Combination of denileukin diftitox and RA significantly suppressed hypoxic HCC cell growth compared to single agent-treated or normoxic cells. Therefore, denileukin diftitox and RA may be therapeutically implicated in infiltrative HCCs which are exposed to hypoxic environments.
그 밖의 정보
- 출판 형태
- Journal Article, Research Support, Non-U.S. Gov't
- 저널
- Cancer letters · eISSN 1872-7980
- 전자 출판
- 2008-11-04
- MeSH
- Blotting, Western · Carcinoma, Hepatocellular / enzymology / pathology · Cell Division / drug effects · Cell Hypoxia · Cell Line, Tumor · Diphtheria Toxin / chemistry / pharmacology · Enzyme Activation · Humans · Interleukin-2 / chemistry / pharmacology · Liver Neoplasms / enzymology / pathology · Mitogen-Activated Protein Kinases / metabolism · Tretinoin / pharmacology
- Substances
- Diphtheria Toxin · Interleukin-2 · Tretinoin · Mitogen-Activated Protein Kinases