Myeloid Cell Leukemia-1 (MCL-1) siRNA Therapy Showed Cytotoxic Effect on T Cells Acute Lymphoblastic Leukemia
Author | Shaghayegh Askarian-Amiri | en |
Author | Farzane Ordoni Aval | en |
Author | Abbas Azadmehr | en |
Author | Morteza Oladnabi | en |
Author | Mahjoobeh Jafari Vesiehsari | en |
Author | Mahmoud Hajiahmadi | en |
Orcid | Mahmoud Hajiahmadi [0000-0001-9721-1629] | en |
Issued Date | 2019-04-30 | en |
Abstract | Background: T-lineage acute lymphoblastic leukemia (T-ALL) is a malignant hyperplastic disease of the hematopoietic system. This tumor is the most common tumor in children and adolescents. Myeloid cell leukemia-1 (Mcl-1) is described as a prosurvival protein from the Bcl2 family. It is an important factor in routine cancer treatments. In fact, in different types of cancers, Mcl-1 downregulation can be a potential target. Objectives: The present study aims to evaluate the cytotoxic effect of MCL-1 siRNA in T-ALL cells. Methods: The present study evaluated the effects of Mcl-1 small interfering RNAs (siRNAs) on survival in Jurkat cells. Specific Mcl-1 siRNA was transfected and using quantitative real-time PCR, the relative expression of Mcl-1 mRNA was determined. Moreover, cell survival was determined using the colorimetric MTT assay. Results: The expression of mRNA reduced effectively in a dose-dependent manner at 48 hours after transfection with Mcl-1 siRNA. In addition, Mcl-1 siRNA treatment could significantly reduce tumor cell survival. Conclusions: Based on the results, downregulation of Mcl-1 by specific siRNAs in T-ALL cells can effectively reduce cell survival. Therefore, Mcl-1 siRNA may be a complementary agent along with standard methods in the treatment of T-ALL. | en |
DOI | https://doi.org/10.5812/ijcm.87773 | en |
Keyword | Mcl-1 | en |
Keyword | siRNA | en |
Keyword | Jurkat Cell Line | en |
Keyword | T-ALL | en |
Publisher | Brieflands | en |
Title | Myeloid Cell Leukemia-1 (MCL-1) siRNA Therapy Showed Cytotoxic Effect on T Cells Acute Lymphoblastic Leukemia | en |
Type | Research Article | en |