Proteomic analysis reveals ATP-dependent steps and chaperones involvement in luteolin-induced lung cancer CH27 cell apoptosis

• Published in: European journal of pharmacology 2010-09, Vol.642 (1), p.19-27
• Main Authors: Lee, Hong-Zin, Yang, Wen-Hui, Bao, Bo-Ying, Lo, Pei-Ling
• Format: Article
• Language: English
• Subjects: 2D electrophoresis; Actin; Actins - metabolism; Adenosine Triphosphate - metabolism; Antineoplastic Agents - pharmacology; Apoptosis - drug effects; Biological and medical sciences; Cell Line, Tumor; Colforsin - pharmacology; Dermatology; Endoplasmic Reticulum - drug effects; Endoplasmic Reticulum - metabolism; Endoplasmic reticulum stress; Gene Expression Regulation, Neoplastic - drug effects; Human lung squamous carcinoma CH27 cell line; Humans; Intracellular Space - drug effects; Intracellular Space - metabolism; Lung Neoplasms - genetics; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Luteolin; Luteolin - pharmacology; Medical sciences; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondron; Molecular Chaperones - metabolism; Pharmacology. Drug treatments; Pneumology; Proteomics; Tumors of the respiratory system and mediastinum; Tumors of the skin and soft tissue. Premalignant lesions
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/j.ejphar.2010.05.053

The present study applied 2D electrophoresis to analyze the proteins involved in luteolin (50 μM)-induced CH27 cell apoptosis. We found 7 proteins to be markedly changed. According to the data of analysis of these protein spots, we hypothesized that ATP synthetic pathway and heat shock proteins were involved in luteolin-induced CH27 cell apoptosis. In this study, luteolin induced a significant change in intracellular ATP levels and mitochondrial activity of CH27 cells. Further experiments demonstrated that pretreatment with forskolin blocked the luteolin-induced cell death. P38 and heat shock protein 27 may be important participants in the luteolin-induced changes in organization of actin microfilaments in this study. In addition, endoplasmic reticulum stress is also important in the luteolin-induced CH27 cell apoptosis. Our findings suggested that the function of mitochondria and endoplasmic reticulum is the integral factor in luteolin-induced CH27 cell apoptosis.