2010•PubMedOpen access

[Effect of Bufalin on proliferation and apoptosis of human non-small cell lung cancer A549 cell].

Zhitu Zhu, Yang Yu, K Wang, Li E, Liu Y, Yunpeng Liu

Open full text 6 citations

Abstract

BACKGROUND AND OBJECTIVE: Bufalin, a component of the Chinese medicine chan'su, induces apoptosis in various human tumor cell lines. The aim of this study is to investigate the mechanism of anti-proliferation and the induction of apoptosis of Bufalin on non-small cell lung cancer cell. METHODS: The effect of Bufalin on A549 cell proliferation was measured using MTT assay; the morphological change was observed with Wright-Giemsa stain; cell cycle phase distribution and hypodiploid DNA were determined by flow cytometry with PI; expressions of Livin, Caspase-3 were detected by Western blot. RESULTS: MTT assay showed that Bufalin inhibited A549 cell proliferation in time and dose-dependent manner. The inhibition concentration of 50% cell growth (IC50) at 48 h, 72 h and 96 h were (56.14+/-6.72) nmol/L, (15.57+/-4.28) nmol/L and (7.39+/-4.16) nmol/L, respectively; apoptosis of A549 cells could be effectively induced by Bufalin; apoptotic bodies and sub-G1 peak (representing apoptosis) emerged when cells were treated with different concentrations, compared with the untreated control group (P < 0.01). The expression of Livin protein was downregulated (P < 0.01) and Caspase-3 protein was activated during Bufalin-induced apoptosis in A549 cells. CONCLUSIONS: Bufalin suppresses the growth of A549 cells and induces apoptosis; inhibition of Livin and activation of Caspase-3 may be involved in its mechanism.

About this research paper

What this paper is about

BACKGROUND AND OBJECTIVE: Bufalin, a component of the Chinese medicine chan'su, induces apoptosis in various human tumor cell lines. The aim of this study is to investigate the mechanism of anti-proliferation and the induction of apoptosis of Bufalin on non-small cell lung cancer cell. METHODS: The effect of Bufalin on A549 cell proliferation was measured using MTT assay; the morphological change was observed with Wright-Giemsa stain; cell cycle phase distribution and hypodiploid DNA were determined by flow cytometry with PI; expressions of Livin, Caspase-3 were detected by Western blot. RESULTS: MTT assay showed that Bufalin inhibited A549 cell proliferation in time and dose-dependent manner. The inhibition concentration of 50% cell growth (IC50) at 48 h, 72 h and 96 h were (56.14+/-6.72) nmol/L, (15.57+/-4.28) nmol/L and (7.39+/-4.16) nmol/L, respectively; apoptosis of A549 cells could be effectively induced by Bufalin; apoptotic bodies and sub-G1 peak (representing apoptosis) emerged when cells were treated with different concentrations, compared with the untreated control group (P < 0.01). The expression of Livin protein was downregulated (P < 0.01) and Caspase-3 protein was activated during Bufalin-induced apoptosis in A549 cells. CONCLUSIONS: Bufalin suppresses the growth of A549 cells and induces apoptosis; inhibition of Livin and activation of Caspase-3 may be involved in its mechanism.

Why it matters

OpenAlex reports 6 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

BACKGROUND AND OBJECTIVE: Bufalin, a component of the Chinese medicine chan'su, induces apoptosis in various human tumor cell lines. The aim of this study is to investigate the mechanism of anti-proliferation and the induction of apoptosis of Bufalin on non-small cell lung cancer cell. METHODS: The effect of Bufalin on A549 cell proliferation was measured using MTT assay; the morphological change was observed with Wright-Giemsa stain; cell cycle phase distribution and hypodiploid DNA were determined by flow cytometry with PI; expressions of Livin, Caspase-3 were detected by Western blot. RESULTS: MTT assay showed that Bufalin inhibited A549 cell proliferation in time and dose-dependent manner. The inhibition concentration of 50% cell growth (IC50) at 48 h, 72 h and 96 h were (56.14+/-6.72) nmol/L, (15.57+/-4.28) nmol/L and (7.39+/-4.16) nmol/L, respectively; apoptosis of A549 cells could be effectively induced by Bufalin; apoptotic bodies and sub-G1 peak (representing apoptosis) emerged when cells were treated with different concentrations, compared with the untreated control group (P < 0.01). The expression of Livin protein was downregulated (P < 0.01) and Caspase-3 protein was activated during Bufalin-induced apoptosis in A549 cells. CONCLUSIONS: Bufalin suppresses the growth of A549 cells and induces apoptosis; inhibition of Livin and activation of Caspase-3 may be involved in its mechanism.

Key concepts: Bufalin, Apoptosis, A549 cell, Cell cycle, Cell growth, Chemistry, MTT assay, Molecular biology

Related papers

Back to paper searchBrowse research topicsOriginal source
[Effect of Bufalin on proliferation and apoptosis of human non-small cell lung cancer A549 cell]. — Research Paper | ScholarLens