期刊
LEUKEMIA RESEARCH
卷 33, 期 1, 页码 109-114出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.leukres.2008.06.023
关键词
Notch; Human chronic myeloid leukemia; K562 cells; Cell proliferation; Colony-forming activity
资金
- National Natural Science Foundation of China [30370598, 30330550, 30425015, 30400079]
- PCSIRT program [IRT0459]
- Ministry of Education of China
- Ministry of Science and Technology of China [2006AA02A111]
Notch signaling functions in the development of some types of leukemia and lymphoma, but the relationship between Notch signaling and chronic myeloid leukemia (CML) remains to be elucidated. In this study, we examined the expression of Notch receptors and ligands in the human CML cell line K562. When the active form of Notch 1, the Notch intra-cellular domain (NIC), was over-expressed in K562, the proliferation of K562 was mildly but significantly inhibited, accompanied by increased Hes 1 mRNA level. On the other hand, when Notch signaling was attenuated by over-expression of a dominant-negative RBP-J, RBP-J(R218H), in K562 cells, the proliferation of K562 was increased. Moreover, we found that activation of Notch signaling inhibited while repression of Notch signaling promoted the colony-forming activity of K562 cells. We examined cell cycle-related molecules in K562 transfected with NIC or RBP-J(R218H), and found that the protein level of the retinoblastoma gene product (the Rb protein) was induced in K562 expressing NIC, and down-regulated in K562 expressing RBP-J(R218H). These data suggest that the Notch signaling may function as a tumor inhibitor in human CML cells. (C) 2008 Elsevier Ltd. All rights reserved.
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