Chemotherapy-Induced Survivin Regulation in Acute Myeloid Leukemia Cells

نویسندگان

چکیده

Survivin is a 16.5 kDa protein highly expressed in centrosomes, where it controls proper sister chromatid separation. In addition to its function mitosis, survivin also involved apoptosis. Overexpression of many cancer types makes suitable target for therapy. Western blotting and confocal microscopy were used characterize the effect chemotherapy on acute myeloid leukemia (AML) cells. We found enhanced expression panel AML cell lines treated with cytarabine (Ara-C), which part first-line induction regimen Simultaneously, Ara-C caused growth arrest depletion mitotic fraction. Subsequently, second component standard therapy protocol, idarubicin, known inhibitor, YM-155, viability localization cells was investigated. Idarubicin reversed Ara-C-induced upregulation majority lines. YM-155 deregulation together decrease resistant idarubicin treatment, suggesting that might be efficient specific subset patients. Expression levels other apoptosis-related proteins, particular X-linked inhibitor apoptosis (XIAP), Mcl-1, p53, cell-cycle p21 considerably changed almost all cases, confirming off-target effects YM-155.

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ژورنال

عنوان ژورنال: Applied sciences

سال: 2021

ISSN: ['2076-3417']

DOI: https://doi.org/10.3390/app11010460