2013Central South PharmacyRequires access

Apoptosis of human lung adenocarcinoma A549 cell line induced by casticin and its mechanism

Xiaona Hu

Open publisher page 0 citations

Abstract

Objective To investigate the apoptosis of human lung adenocarcinoma cancer A549 cells induced by casticin(CAS) and the mechanism. Methods The inhibitory effect of CAS on the proliferation of A549 cells was measured by agar colony formation assay. CAS-induced apoptosis rates of A549 cells were observed by flow cytometry(FCM) with propidium iodide staining. The cell apoptosis morphology was observed by AO/EB fluorescence staining. FoxM1 expression was analyzed by Western blot. Results CAS had a significantly inhibitory effect on the cell proliferation in A549 cells in a concentration-dependent manner, and the IC50was 7.26 μmol L- 1. CAS treated A549 cells presented typical apoptotic morphology, and CAS induced the apoptosis of A549 cells in a concentration-dependent manner. Western blot demonstrated that expression of FoxM1 was down-regulated in a concentration-time-dependent manner. Conclusion CAS can inhibit the proliferation of A549 cells and induce the apoptosis of A549 cells, which may be due to the down-regulation of FoxM1 expression.

About this research paper

What this paper is about

Objective To investigate the apoptosis of human lung adenocarcinoma cancer A549 cells induced by casticin(CAS) and the mechanism. Methods The inhibitory effect of CAS on the proliferation of A549 cells was measured by agar colony formation assay. CAS-induced apoptosis rates of A549 cells were observed by flow cytometry(FCM) with propidium iodide staining. The cell apoptosis morphology was observed by AO/EB fluorescence staining. FoxM1 expression was analyzed by Western blot. Results CAS had a significantly inhibitory effect on the cell proliferation in A549 cells in a concentration-dependent manner, and the IC50was 7.26 μmol L- 1. CAS treated A549 cells presented typical apoptotic morphology, and CAS induced the apoptosis of A549 cells in a concentration-dependent manner. Western blot demonstrated that expression of FoxM1 was down-regulated in a concentration-time-dependent manner. Conclusion CAS can inhibit the proliferation of A549 cells and induce the apoptosis of A549 cells, which may be due to the down-regulation of FoxM1 expression.

Why it matters

A significance statement is not available in the OpenAlex record.

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

Objective To investigate the apoptosis of human lung adenocarcinoma cancer A549 cells induced by casticin(CAS) and the mechanism. Methods The inhibitory effect of CAS on the proliferation of A549 cells was measured by agar colony formation assay. CAS-induced apoptosis rates of A549 cells were observed by flow cytometry(FCM) with propidium iodide staining. The cell apoptosis morphology was observed by AO/EB fluorescence staining. FoxM1 expression was analyzed by Western blot. Results CAS had a significantly inhibitory effect on the cell proliferation in A549 cells in a concentration-dependent manner, and the IC50was 7.26 μmol L- 1. CAS treated A549 cells presented typical apoptotic morphology, and CAS induced the apoptosis of A549 cells in a concentration-dependent manner. Western blot demonstrated that expression of FoxM1 was down-regulated in a concentration-time-dependent manner. Conclusion CAS can inhibit the proliferation of A549 cells and induce the apoptosis of A549 cells, which may be due to the down-regulation of FoxM1 expression.

Key concepts: A549 cell, Apoptosis, Propidium iodide, Flow cytometry, Chemistry, Western blot, Molecular biology, Cell growth

Related papers

Back to paper searchBrowse research topicsOriginal source
Apoptosis of human lung adenocarcinoma A549 cell line induced by casticin and its mechanism — Research Paper | ScholarLens