Department of Biological Sciences, Institute for Advanced Studies in Basic Sciences (IASBS), 45137-66731, Zanjan, Iran.
Laboratory for Functional and Metabolic Imaging, Institute of Physics, Swiss Federal Institute of Technology (EPFL), Station6, 1015, Lausanne, Switzerland.
Mol Cell Biochem. 2023 Nov;478(11):2435-2444. doi: 10.1007/s11010-023-04671-w. Epub 2023 Feb 18.
Vimentin is a main type 3 intermediate filament protein. It seems that abnormal expression of vimentin is contributed to the appearance of the aggressive feature of cancer cells. So that it has been reported that malignancy and epithelial-mesenchymal transition in solid tumors, and poor clinical outcomes in patients with lymphocytic leukemia and acute myelocytic leukemia have been associated with the high expression of vimentin. Vimentin is a non-caspase substrate of caspase-9 although its cleavage by caspase-9 in biological processes has not been reported. In the present study, we sought to understand whether vimentin cleavage mediated by caspase-9 could reverse the malignancy in leukemic cells. Herein, to address the issue, we investigated vimentin changes in differentiation and took advantage of the inducible caspase-9 (iC9)/AP1903 system in human leukemic NB4 cells. Following the transfection and treatment of the cells using the iC9/AP1903 system, vimentin expression, cleavage, and subsequently, the cell invasion and the relevant markers such as CD44 and MMP-9 were evaluated. Our results revealed the downregulation and cleavage of vimentin which attenuates the malignant phenotype of the NB4 cells. Considering the favorable effect of this strategy in keeping down the malignant features of the leukemic cells, the effect of the iC9/AP1903 system in combination with all-trans-retinoic acid (ATRA) treatment was evaluated. The obtained data prove that iC9/AP1903 significantly makes the leukemic cells more sensitive to ATRA.
波形蛋白是主要的中间丝蛋白类型 3。似乎波形蛋白的异常表达导致了癌细胞侵袭特征的出现。因此,已经有报道称,实体瘤中的恶性肿瘤和上皮间质转化,以及淋巴细胞性白血病和急性髓细胞性白血病患者的不良临床结局与波形蛋白的高表达有关。尽管波形蛋白是 caspase-9 的非半胱天冬酶底物,但在生物过程中尚未报道其被 caspase-9 切割。在本研究中,我们试图了解 caspase-9 介导的波形蛋白切割是否可以逆转白血病细胞的恶性程度。为此,我们研究了分化过程中波形蛋白的变化,并利用人白血病 NB4 细胞中的诱导型 caspase-9(iC9)/AP1903 系统。在使用 iC9/AP1903 系统转染和处理细胞后,评估了波形蛋白的表达、切割以及随后的细胞侵袭和相关标志物,如 CD44 和 MMP-9。我们的结果显示,波形蛋白的下调和切割减弱了 NB4 细胞的恶性表型。考虑到这种策略在保持白血病细胞恶性特征方面的有利效果,评估了 iC9/AP1903 系统与全反式维甲酸(ATRA)治疗的联合效果。获得的数据证明 iC9/AP1903 使白血病细胞对 ATRA 更敏感。