Aichberger Karl J, Mayerhofer Matthias, Gleixner Karoline V, Krauth Maria-Theresa, Gruze Alexander, Pickl Winfried F, Wacheck Volker, Selzer Edgar, Müllauer Leonhard, Agis Hermine, Sillaber Christian, Valent Peter
Department of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Austria.
Blood. 2007 Apr 1;109(7):3031-41. doi: 10.1182/blood-2006-07-032714.
MCL-1 is a Bcl-2 family member that has been described as antiapoptotic in various myeloid neoplasms. Therefore, MCL-1 has been suggested as a potential new therapeutic target. Systemic mastocytosis (SM) is a myeloid neoplasm involving mast cells (MCs) and their progenitors. In the present study, we examined the expression and functional role of MCL-1 in neoplastic MCs and sought to determine whether MCL-1 could serve as a target in SM. As assessed by RT-PCR and immunohistochemical examination, primary neoplastic MCs expressed MCL-1 mRNA and the MCL-1 protein in all SM patients examined. Moreover, MCL-1 was detectable in both subclones of the MC line HMC-1--HMC-1.1 cells, which lack the SM-related KIT mutation D816V, and HMC-1.2 cells, which carry KIT D816V. Exposure of HMC-1.1 cells or HMC-1.2 cells to MCL-1-specific antisense oligonucleotides (ASOs) or MCL-1-specific siRNA resulted in reduced survival and increased apoptosis compared with untreated cells. Moreover, MCL-1 ASOs were found to cooperate with various tyrosine kinase inhibitors in producing growth inhibition in neoplastic MCs, with synergistic effects observed with PKC412, AMN107, and imatinib in HMC-1.1 cells and with PKC412 in HMC-1.2 cells. Together, these data show that MCL-1 is a novel survival factor and an attractive target in neoplastic MCs.
MCL-1是一种Bcl-2家族成员,在多种髓系肿瘤中被描述为具有抗凋亡作用。因此,MCL-1被认为是一个潜在的新治疗靶点。系统性肥大细胞增多症(SM)是一种涉及肥大细胞(MCs)及其祖细胞的髓系肿瘤。在本研究中,我们检测了MCL-1在肿瘤性MCs中的表达及功能作用,并试图确定MCL-1是否可作为SM的治疗靶点。通过逆转录聚合酶链反应(RT-PCR)和免疫组化检测评估,在所检测的所有SM患者中,原发性肿瘤性MCs均表达MCL-1 mRNA和MCL-1蛋白。此外,在MC系HMC-1的两个亚克隆中均可检测到MCL-1,其中HMC-1.1细胞缺乏与SM相关的KIT突变D816V,而HMC-1.2细胞携带KIT D816V。与未处理的细胞相比,将HMC-1.1细胞或HMC-1.2细胞暴露于MCL-1特异性反义寡核苷酸(ASOs)或MCL-1特异性小干扰RNA(siRNA)会导致细胞存活率降低和凋亡增加。此外,发现MCL-1 ASOs与多种酪氨酸激酶抑制剂协同作用,可抑制肿瘤性MCs的生长,在HMC-1.1细胞中与PKC412、AMN107和伊马替尼联合使用时观察到协同效应,在HMC-1.2细胞中与PKC412联合使用时也观察到协同效应。总之,这些数据表明MCL-1是肿瘤性MCs中的一种新型存活因子和有吸引力的治疗靶点。