Acacetin-induced cell cycle arrest and apoptosis in human non-small cell lung cancer A549 cells.

Abstract

In this study, we examined acacetin (5,7-dihydroxy-4'-methoxyflavone), a flavonoid compound, for its effect on proliferation in human non-small cell lung cancer A549 cells. The results first reported that acacetin not only inhibited A549 cell proliferation but also induced apoptosis and blocked cell cycle progression in the G1 phase. ELISA assay demonstrated that acacetin significantly increased the expression of p53 and p21/WAF1 protein, which caused cell cycle arrest. An enhancement in Fas and its two forms of ligands, membrane-bound Fas ligand (mFasL) and soluble Fas ligand (sFasL), might be responsible for the apoptotic effect induced by acacetin. Taken together, p53 and Fas/FasL apoptotic system may participate in the antiproliferative activity of acacetin in A549 cells.

• Authors: Ya-Ling Hsu, Po-Lin Kuo, Chi-Feng Liu, Chun-Ching Lin
• Journal: Cancer letters (Cancer Lett) Vol. 212 Issue 1 Pg. 53-60 (Aug 20 2004) ISSN: 0304-3835 [Print] Ireland
• PMID: 15246561 (Publication Type: Journal Article)

Chemical References

• Antigens, Surface
• CDKN1A protein, human
• Cyclin-Dependent Kinase Inhibitor p21
• Cyclins
• FASLG protein, human
• Fas Ligand Protein
• Flavones
• Flavonoids
• Membrane Glycoproteins
• Tumor Suppressor Protein p53
• fas Receptor
• acacetin

Topics

• Antigens, Surface
• Apoptosis (drug effects)
• Carcinoma, Non-Small-Cell Lung (pathology)
• Cell Cycle (drug effects)
• Cell Division (drug effects)
• Cyclin-Dependent Kinase Inhibitor p21
• Cyclins (biosynthesis)
• Enzyme-Linked Immunosorbent Assay
• Fas Ligand Protein
• Flavones
• Flavonoids (pharmacology)
• Humans
• Lung Neoplasms (pathology)
• Membrane Glycoproteins (pharmacology)
• Tumor Cells, Cultured
• Tumor Suppressor Protein p53 (biosynthesis)
• fas Receptor