2007•Shiyong yixue zazhiRequires access

Combination of survivin and bcl-2 antisense oligodeoxynucleotides in the induction of K562 cell apoptosis

BI Fu-yon

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Abstract

Objective To explore the synergistic effect of survivin and bcl-2 antisense oligodeoxynucleotide(ASODN) on the induction of K562 cell apoptosis. Methods The ASODNs were transfected into K562 cells by the vector LipofectamineTM2000. There were six groups in this experiment:control group, lipo group, NODN group, survivin ASODN group, bcl-2 ASODN group, and combination group. MTT assay was used to determine cell proliferation. The rate of cell apoptosis was detected by FCM. The expression of survivin mRNA was evaluated with semi-quantitative RT-PCR. Results The inhibitory rate of K562 cell was significant higher in the combination group than in survivin ASODN or bcl-2 ASODN group (60.98% vs. 48.78% or 60.98% vs. 40.24%, P 0.01). Either survivin ASODN or bcl-2 ASODN could induce K562 cell apoptosis with a apoptotic rate of (13.36 ± 4.03)% or (10.40 ± 1.71)% and the rate elevated to (26.14 ± 4.39)% for the combination of survivin ASODN and bcl-2 ASODN (P 0.01). The level of survivin mRNA in the combination group was markedly lower than that in survivin ASODN or bcl-2 ASODN group. Conclusion The combination of survivin and bcl-2 ASODN synergistically inhibits the proliferation of K562 cells and increases cell apoptosis, providing a new gene therapy for leukemia.

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Objective To explore the synergistic effect of survivin and bcl-2 antisense oligodeoxynucleotide(ASODN) on the induction of K562 cell apoptosis. Methods The ASODNs were transfected into K562 cells by the vector LipofectamineTM2000. There were six groups in this experiment:control group, lipo group, NODN group, survivin ASODN group, bcl-2 ASODN group, and combination group. MTT assay was used to determine cell proliferation. The rate of cell apoptosis was detected by FCM. The expression of survivin mRNA was evaluated with semi-quantitative RT-PCR. Results The inhibitory rate of K562 cell was significant higher in the combination group than in survivin ASODN or bcl-2 ASODN group (60.98% vs. 48.78% or 60.98% vs. 40.24%, P 0.01). Either survivin ASODN or bcl-2 ASODN could induce K562 cell apoptosis with a apoptotic rate of (13.36 ± 4.03)% or (10.40 ± 1.71)% and the rate elevated to (26.14 ± 4.39)% for the combination of survivin ASODN and bcl-2 ASODN (P 0.01). The level of survivin mRNA in the combination group was markedly lower than that in survivin ASODN or bcl-2 ASODN group. Conclusion The combination of survivin and bcl-2 ASODN synergistically inhibits the proliferation of K562 cells and increases cell apoptosis, providing a new gene therapy for leukemia.

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Available abstract

Objective To explore the synergistic effect of survivin and bcl-2 antisense oligodeoxynucleotide(ASODN) on the induction of K562 cell apoptosis. Methods The ASODNs were transfected into K562 cells by the vector LipofectamineTM2000. There were six groups in this experiment:control group, lipo group, NODN group, survivin ASODN group, bcl-2 ASODN group, and combination group. MTT assay was used to determine cell proliferation. The rate of cell apoptosis was detected by FCM. The expression of survivin mRNA was evaluated with semi-quantitative RT-PCR. Results The inhibitory rate of K562 cell was significant higher in the combination group than in survivin ASODN or bcl-2 ASODN group (60.98% vs. 48.78% or 60.98% vs. 40.24%, P 0.01). Either survivin ASODN or bcl-2 ASODN could induce K562 cell apoptosis with a apoptotic rate of (13.36 ± 4.03)% or (10.40 ± 1.71)% and the rate elevated to (26.14 ± 4.39)% for the combination of survivin ASODN and bcl-2 ASODN (P 0.01). The level of survivin mRNA in the combination group was markedly lower than that in survivin ASODN or bcl-2 ASODN group. Conclusion The combination of survivin and bcl-2 ASODN synergistically inhibits the proliferation of K562 cells and increases cell apoptosis, providing a new gene therapy for leukemia.

Key concepts: Survivin, Apoptosis, K562 cells, Transfection, Molecular biology, Cell growth, Cell, Cancer research

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