Growth Inhibition and Apoptosis Induction of Sulindac on Human Lung Cancer Cells.
10.4046/trd.2004.56.5.514
- Author:
Hak Ryul KIM
1
;
Sei Hoon YANG
;
Eun Taik JEONG
Author Information
1. Department of Internal Medicne, Wonkwang University College of Medicne, Iksan, Korea. yshpul@wonkwang.ac.kr
- Publication Type:Original Article
- Keywords:
Lung cancer;
Sulindac;
Apoptosis
- MeSH:
Apoptosis*;
Carcinoma, Non-Small-Cell Lung;
Cell Death;
Cell Line;
Chemoprevention;
Chromatin;
Colonic Neoplasms;
Colorectal Neoplasms;
Humans*;
Lactic Acid;
Lung Neoplasms*;
Lung*;
Sulindac*
- From:Tuberculosis and Respiratory Diseases
2004;56(5):514-522
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAID) are useful in chemoprevention of colorectal cancers. Continuous NSAID administation causes 40% to 50% reduction in relative risk for colorectal cancer. Sulindac possesses an antiproliferative effect and induces apoptosis and tumor regression on colon cancer and other types of cancers. We intended to analyze the effects of sulindac in three non-small cell lung cancer cell lines. MATERIALS AND METHODS: The human lung cancer cell lines, A549, NCI-H157 and NCI-H460 were used for this study. Viability was tested by MTT assay, and cell death rate was measured by lactate dehydrogenase(LDH) release. Apoptosis was estimated by flow cytometric analysis and nuclear staining. RESULTS: Sulindac was able to decrease the viability of non-small cell lung cancer cells in a dose- and time- dependent manner. In a parallel effect of sulindac on cell death rate, LDH release was increased in sulindac-treated lung cancer cells. Sulindac significantly increased apoptosis characterized by an increase of sub-G0/G1 fraction and morphological change of nuclei. The rate of apoptotic cells after sulindac treatment in lung cancer cells increased in a time- and dose- dependent manner in flow cytometric analysis. Apoptotic cells were defined as nuclear shrinkage, chromatin condensation and nuclear fragmentation of cells. CONCLUSION: Sulindac decreases viability and induces the apoptosis of lung cancer cells. Further studies will be needed to elucidate the potential mechanism of sulindac-induced apoptosis in lung cancer cells.
