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Effects of lentivirus mediated STAT3 silencing on human chronic myeloid leukemia cells and leukemia mice
Xinyan Jia1, Wenzhong Yang1, Jia Han2
1Department of Hematology, East Hospital, Tongji University School of Medicine Shanghai 200120, China.
Objective:
To investigate the effects of lentivirus mediated STAT3 silencing on human chronic myeloid leukemia cells (K562) and the growth of chronic myeloid leukemia mice as well as to explore the potential mechanisms.
Methods:
Unbtreated K562 cells (CON), blank lentivirus transfected K562 cells (NC) and K562 cells expressing STAT3 siRNA (STAT3 siRNA) were injected into SCID mice to establish the chronic myeloid leukemia model in mice. The growth, peripheral white blood cell count and spleen index in these mice were determined.
Results:
In vitro experiment showed, when compared with control group, the interference efficiency of STAT3 expression was as high as 97.5% in K562 cells. Western blot assay revealed that the expression of c-Myc, Bcl-xL and Cyclin D1 reduced by 17.01%, 7.3% and 6.82%, respectively, showing significant difference when compared with control group (P < 0.01). These findings were consistent with those from fluorescence quantitative PCR. In vivo experiment showed the body weight of mice reduced progressively and the peripheral white blood cell count increased gradually in control group, accompanied by dragging hind limbs and progressive enlargement of the spleen. The body weight remained unchanged, peripheral white blood cell count reduced gradually and the spleen did not enlarge in mice treated with STAT3 siRNA expressing cells.
Conclusion:
Lentivirus mediated STAT3 silencing may inhibit the expression of its downstream genes (c-Myc, Bcl-xL and Cyclin D1) related to cell proliferation, apoptosis and cycle to suppress the malignant biological behaviors, and STAT3 silencing also inhibit the leukemogenic potency of K562 cells in mice.
Insights
Lentivirus-mediated STAT3 silencing effectively suppressed chronic myeloid leukemia (CML) cell growth and reduced tumor progression in mice. This approach targets key genes involved in cell proliferation and survival, offering a potential therapeutic strategy for CML.
Area of Science:
- Oncology
- Molecular Biology
- Gene Therapy
Background:
- Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by uncontrolled proliferation of myeloid cells.
- STAT3 signaling pathway plays a crucial role in the pathogenesis and progression of various cancers, including CML.
Purpose of the Study:
- To investigate the therapeutic potential of lentivirus-mediated STAT3 silencing in K562 CML cells and a CML mouse model.
- To elucidate the underlying molecular mechanisms of STAT3 inhibition in CML.
Main Methods:
- Establishment of a CML mouse model using K562 cells with STAT3 siRNA lentivirus.
- In vitro assessment of STAT3 silencing efficiency and downstream gene expression (c-Myc, Bcl-xL, Cyclin D1) in K562 cells.
- In vivo monitoring of tumor growth, peripheral white blood cell count, and spleen index in treated and control mice.
Main Results:
- STAT3 silencing achieved over 97% interference efficiency in K562 cells.
- Significant reduction in c-Myc, Bcl-xL, and Cyclin D1 expression observed post-STAT3 silencing.
- In vivo studies demonstrated suppressed tumor growth, normalized white blood cell counts, and reduced spleen enlargement in mice treated with STAT3-silenced cells.
Conclusions:
- Lentivirus-mediated STAT3 silencing effectively inhibits CML progression by downregulating key genes involved in cell proliferation, apoptosis, and cell cycle.
- STAT3 silencing demonstrates significant anti-leukemic activity, suggesting its potential as a therapeutic target for CML.
