Small hairpin RNA targeting at Bcl-2 increases cytarabine-induced apoptosis in Raji cells

He, Dalin; Fang, Baoying

doi:10.1093/abbs/gmn015

Cited by 7 publications

(5 citation statements)

References 17 publications

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“…Previous studies have shown that a reduction in BCL2 expression by siRNA is capable of inducing apoptosis in Raji cells (12). In the present study, as expected, BCL11A siRNA treatment in combination with BCL2 siRNA decreased cell proliferation and increased the number of apoptotic cells compared with BCL11A or BCL2 siRNA-transfected cells alone.…”

Section: Discussionsupporting

confidence: 89%

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Downregulation of BCL11A by siRNA induces apoptosis in B lymphoma cell lines

Gao

et al. 2012

Biomedical Reports

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Abstract. The B-cell chronic lymphocytic leukemia (CLL)/lymphoma 11A gene (BCL11A) encodes a krüppel-like zinc finger protein, which is important in thymopoiesis and has been associated with hematopoietic malignancies. In this study, we investigated whether the downregulation of BCL11A mRNA by small interference RNA (siRNA) was capable of inducing apoptosis, and tested the effect of BCL11A siRNA combined with BCL2 siRNA in B lymphoma cell lines (SUDHL6, EB1). BCL11A siRNA was transfected into SUDHL6, EB1 cells with HiPerfect transfection reagents. After transient transfection with BCL11A siRNA, the expression levels of BCL11A mRNA and protein were assayed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analysis. The cell proliferation was determined by a cell counting kit-8 (CCK8) assay. Apoptosis was determined by morphological observation and flow cytometric analysis. The results showed that the expression levels of BCL11A mRNA and protein from SUDHL6, EB1 cells transfected with BCL11A siRNA decreased, compared with either the scrambled negative control siRNA group or untransfected cells group (P<0.05). Viability of cells transfected with BCL11A siRNA was less compared to cells transfected with control siRNA and untransfected SUDHL6, EB1 cells, respectively (P<0.05). BCL11A siRNA induced apoptosis in both SUDHL6 and EB1 cells. BCL11A siRNA combined with BCL2 siRNA significantly inhibited cell growth. Apoptotic rates of SUDHL6, EB1 cells treated with BCL11A siRNA combined with BCL2 siRNA significantly increased (P<0.05), compared with either the scrambled control (Sc) siRNA and BCL2 siRNA combination or BCL2 or BCL11A siRNA-treated cells alone. Findings of this study suggest the downregulation of BCL11A mRNA by siRNA was able to induce apoptosis.Moreover, BCL11A siRNA combined with BCL2 siRNA increased apoptosis in SUDHL6, EB1 cells. Thus, suppression of BCL11A expression may be a useful approach in the treatment of B lymphoma.

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Section: Discussionsupporting

confidence: 89%

“…It has been shown that siRNA targeting against BCL2 mRNA was able to effectively induce apoptosis of lymphoma and leukemia cells (11)(12)(13). However, whether BCL11A siRNA combined with BCL2 siRNA enhanced apoptosis of lymphoma SUDHL6, EB1 cells remains uncertain.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of BCL11A by siRNA induces apoptosis in B lymphoma cell lines

Gao

et al. 2012

Biomedical Reports

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“…Our previous studies and other groups have suggested that downregulation of BCL-2 expression by siRNA increases the sensitivity of human tumor cells to chemotherapeutic drugs [28-30]. MDM2 negatively regulates the activity of the tumor suppressor protein p53, thus having an anti-apoptotic role [31].…”

Section: Resultsmentioning

confidence: 99%

Combination of BCL11A siRNA with vincristine increases the apoptosis of SUDHL6 cells

Ding

et al. 2014

Eur J Med Res

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BackgroundB cell chronic lymphocytic leukemia/lymphoma 11 A (BCL11A) is associated with human B cell malignancy initiation. Our previous study has shown that downregulation of BCL11A mRNA by small interfering RNA (siRNA) is capable of inducing apoptosis in the SUDHL6 cell line. To further explore the effects of BCL11A siRNA on the enhanced cytotoxicity of a chemotherapeutic drug, we investigated the effects of BCL11A siRNA combined with vincristine (VCR) on SUDHL6 cell proliferation and apoptosis.MethodsChemically synthesized BCL11A siRNA was transfected into SUDHL6 cells using the HiPerFect Transfection Reagent in combination with VCR. Cell proliferation was measured by the CCK8 assay. The morphology of apoptotic cells was observed with Hoechst 33258 staining. The rate of cell apoptosis was determined by annexin V-fluorescein isothiocyanate/propidium iodide double staining using fluorescence-activated cell sorting (FACS) analysis.ResultsAfter BCL11A siRNA plus VCR treatment, cell proliferation was significantly decreased in comparison with VCR or BCL11A siRNA treatment alone and negative control siRNA plus VCR treatment (P <0.05). The apoptotic rate of BCL11A siRNA plus VCR treated cells was significantly increased compared with BCL11A siRNA and VCR treatment alone and negative control siRNA plus VCR treatment (P <0.05).ConclusionsThe combination of BCL11A siRNA and VCR increases apoptosis in SUDHL6 cells. Our study implies that BCL11A siRNA in combination with VCR may be a useful approach for improving effective treatment for B cell lymphoma.

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“…Therefore, agents that target one or both of the two factors are able to induce apoptosis and are considered to be the potential drugs that can be used to treat Burkitt lymphoma [12, 18, 19]. Moreover, icaritin shows the ability to decrease the level of Bcl-2 and c-Myc proteins in several studies [2, 4, 8, 9].…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic Effect of Icaritin and Its Mechanisms in Inducing Apoptosis in Human Burkitt Lymphoma Cell Line

Yao

Liu

et al. 2014

BioMed Research International

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Icaritin (ICT), a hydrolytic product of icariin from Epimedium genus, exhibits antitumor activities in several human solid-tumor and myeloid leukemia cells with extensive influence on various cell signal molecules, such as MAPKs being involved in cell proliferation and Bcl-2 participating in cell apoptosis. However, the effect of icaritin on Burkitt Lymphoma has not been elucidated. In the present study, we first screened the potential effect of icaritin on Burkitt lymphoma Raji and P3HR-1 cell lines and found that icaritin showed cytotoxicity in both cell lines. We further found that icaritin could significantly inhibit Raji cells proliferation with S-phase arrest of cell cycle and induced cell apoptosis accompanied by activation of caspase-8 and caspase-9 and cleavage of PARP. We also observed that icaritin was able to decrease Bcl-2 levels, thus shifting the Bcl-2/Bax ratio, and it could obviously reduce c-Myc, a specific molecular target in Burkitt lymphoma. Our findings demonstrated that icaritin showed cytotoxicity, inhibited cell growth, caused S arrest, and induced apoptosis in Burkitt lymphoma cells and provided a rationale for the further evaluation of icaritin for Burkitt lymphoma therapy.

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Small hairpin RNA targeting at Bcl-2 increases cytarabine-induced apoptosis in Raji cells

Cited by 7 publications

References 17 publications

Downregulation of BCL11A by siRNA induces apoptosis in B lymphoma cell lines

Downregulation of BCL11A by siRNA induces apoptosis in B lymphoma cell lines

Combination of BCL11A siRNA with vincristine increases the apoptosis of SUDHL6 cells

Cytotoxic Effect of Icaritin and Its Mechanisms in Inducing Apoptosis in Human Burkitt Lymphoma Cell Line

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