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ISOLIQUIRITIGENIN INHIBITS THE PROLIFERATION AND INDUCES THE APOPTOSIS OF HUMAN NON‐SMALL CELL LUNG CANCER A549 CELLS
Author(s) -
Hsu YaLing,
Kuo PoLin,
Chiang LienChai,
Lin ChunChing
Publication year - 2004
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2004.04016.x
Subject(s) - isoliquiritigenin , fas ligand , apoptosis , a549 cell , cell growth , cell cycle , chemistry , cancer research , cell cycle checkpoint , chalcone , cell culture , cell , microbiology and biotechnology , biology , programmed cell death , biochemistry , stereochemistry , genetics
SUMMARY 1. Isoliquiritigenin (ISL) is a natural pigment with the simple chalcone structure 4,2′,4′‐trihydroxychalcone. In the present study, we report, for the first time, ISL‐induced inhibition of the proliferation of the human non‐small cell lung cancer A549 cell line. 2. The results showed that ISL not only inhibited A549 cell proliferation, but also induced apoptosis and blocked cell cycle progression in the G1 phase. An ELISA assay demonstrated that ISL significantly increased the expression of p53 and p21/WAF1 protein, which caused cell cycle arrest. 3. An enhancement in Fas and its two ligands, namely membrane‐bound Fas ligand (mFasL) and soluble Fas ligand (sFasL), may be responsible for the apoptotic effect induced by ISL. 4. Taken together, the results indicate that the p53 and Fas/FasL apoptotic system may participate in the antiproliferative activity of ISL in A549 cells.