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Biological effects of decreasing RBM15 on chronic myelogenous leukemia cells
Yuxia Yang1, Saifeng Wang, Yanju Zhang
1Department of Medical Genetics, Peking University, Beijing, China. yangyx@bjmu.edu.cn
Abstract:
RNA binding motif protein 15 (RBM15) was originally described as a 5' translocation partner of the MAL gene in t(1;22)(p13;q13)infant acute megakaryocytic leukemia. Although previous investigations have shown that Rbm15 has broad regulatory effects within murine hematopoiesis through modulating Notch-induced transcriptional activation, which plays key roles in leukemogenesis, it is not clear what the functions of RBM15 are in the regulation of hematological malignancies. In the present study, we show that RBM15 expression was significantly increased in patients with blast-crisis chronic myelogenous leukemia (CML) compared with chronic-phase or accelerated-phase disease by real-time reverse transcription-polymerase chain reaction (RT-PCR) assay. To further elucidate the role of RBM15 in CML, we introduced RBM15 small interfering RNA (siRNA) using pSUPER into CML cells. Fluorescence activated cell sorting (FACS), real-time RT-PCR and Western blot were used to study changes in RBM15 expression levels in transduced cells by comparing with control cells. Decreasing RBM15 levels with RNA interference could inhibit the growth and proliferation, block the cell cycle and induce apoptosis in CML cells. Knockdown of RBM15 may also act to inhibit clonogenicity and induce differentiation of CML cells along the myeloid lineage. Our studies also show that the effects of RBM15 on CML cells may be mediated, at least in part, via its effect on Notch signaling. These findings demonstrate that RBM15 does indeed play a critical role in the survival of CML cells, which may have potential application in designing molecular therapies for CML treatment.
Insights
RNA binding motif protein 15 (RBM15) is elevated in chronic myelogenous leukemia (CML) blast crisis. Reducing RBM15 inhibits CML cell growth and survival, suggesting it as a therapeutic target.
Area of Science:
- Hematology
- Molecular Biology
- Oncology
Background:
- RNA binding motif protein 15 (RBM15) has known regulatory roles in murine hematopoiesis.
- The specific function of RBM15 in hematological malignancies, particularly chronic myelogenous leukemia (CML), remains unclear.
Purpose of the Study:
- To investigate the role of RBM15 in the pathogenesis and progression of CML.
- To evaluate the therapeutic potential of targeting RBM15 in CML.
Main Methods:
- Real-time reverse transcription-polymerase chain reaction (RT-PCR) to quantify RBM15 expression in CML patients.
- RNA interference (siRNA) to reduce RBM15 levels in CML cells.
- Flow cytometry (FACS), RT-PCR, and Western blot to assess cellular changes post-RBM15 knockdown.
Main Results:
- RBM15 expression is significantly increased in blast-crisis CML compared to other phases.
- RBM15 knockdown inhibited CML cell growth, proliferation, and clonogenicity.
- RBM15 depletion induced cell cycle arrest, apoptosis, and myeloid differentiation in CML cells.
- RBM15's effects on CML cells appear to involve modulation of Notch signaling.
Conclusions:
- RBM15 plays a critical role in the survival and progression of CML.
- Targeting RBM15 represents a potential molecular therapy strategy for CML treatment.
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