p21(Cip1) 赋予人类慢性髓性白血病细胞对伊马替尼的耐药性。
p21(Cip1) confers resistance to imatinib in human chronic myeloid leukemia cells.
机构信息
Departamento de Biología Molecular, Facultad de Medicina, Instituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC-IDICAN, Santander, Spain.
出版信息
Cancer Lett. 2010 Jun 1;292(1):133-9. doi: 10.1016/j.canlet.2009.11.017. Epub 2009 Dec 29.
Imatinib is a Bcr-Abl inhibitor used as first-line therapy of chronic myeloid leukemia (CML). p21(Cip1), initially described as a cell cycle inhibitor, also protects from apoptosis in some models. We describe that imatinib down-regulates p21(Cip1) expression in CML cells. Using K562 cells with inducible p21 expression and transient transfections we found that p21 confers partial resistance to imatinib-induced apoptosis. This protection is not related to the G2-arrest provoked by p21, a decrease in the imatinib activity against Bcr-Abl or a cytoplasmic localization of p21. The results suggest an involvement of p21(Cip1) in the response to imatinib in CML.
伊马替尼是一种用于慢性髓性白血病（CML）一线治疗的 Bcr-Abl 抑制剂。最初被描述为细胞周期抑制剂的 p21（Cip1），在某些模型中也能防止细胞凋亡。我们描述了伊马替尼可下调 CML 细胞中 p21（Cip1）的表达。使用具有诱导性 p21 表达的 K562 细胞和瞬时转染，我们发现 p21 赋予了对伊马替尼诱导的细胞凋亡的部分抗性。这种保护与 p21 引起的 G2 期阻滞无关，也与伊马替尼对 Bcr-Abl 的活性降低或 p21 的细胞质定位无关。结果表明，p21（Cip1）参与了 CML 对伊马替尼的反应。
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