Poster Presentations: Wednesday, November 3, 2010 |

Cytokines Cause Apoptosis of Lung Adenocarcinoma Cells Treated With Talc FREE TO VIEW

Pyng Lee, MD; Sun Li, PhD; Swee Eng Aw, MD
Author and Funding Information

National University Hospital, Singapore, Singapore

Chest. 2010;138(4_MeetingAbstracts):515A. doi:10.1378/chest.10370
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PURPOSE: We previously reported that talc caused selective apoptosis of lung adenocarcinoma cells in a dose and time dependent fashion. This study aims to determine if cytokines could be a possible mechanism for cancer cell apoptosis.

METHODS: Fine particle talc (< 2&#181m) is prepared using density gradient, dried, weighted and reconstituted in suspension at 1mg/ml. Commercial lung adenocarcinoma cell line A549 is cultured at 105/ml in 6-well plates containing RPMI1640 with 10% fetal calf serum and incubated at 37 degC, 5% CO2 and 100% humidity. Talc suspension at increasing concentrations 25, 50 and 75 &#181g/ml are added to A549 cell cultures. Controls are lung adenocarcinoma cells (A549) without administration of talc. Quantitative measurements of TNF-α, IL-1β, IL-6, IL-8, IL-10, IL-12p70, soluble CD30, CD40-Ligand , G-CSF, soluble Platelet-Endothelial cell adhesion molecule-1 and soluble vascular cell adhesion molecule-1 (sVCAM-1) in the culture supernatant of controls and talc-treated A549 cells are performed using Cytometric Bead Array (Becton-Dickinson(tm) and Bender MedSystems(r)) at 24, 48 and 72 hours.

RESULTS: Lung adenocarcinoma cells produce baseline low levels of IL-6 and IL8. With talc treatment, higher concentrations of IL-6 and IL-8 as well as release of G-CSF, sVCAM and CD40-Ligand are observed in a time- and dose-dependent fashion (figures 1,1a). These cytokines are mediators for a variety of immune and inflammatory responses.

CONCLUSION: Increase in IL-6 and IL-8 from baseline as well as release of other pro-inflammatory cytokines suggest that talc induced apoptosis of human lung adenocarcinoma cells could be mediated through a specific combination of pro-inflammatory cytokines and chemokines.

CLINICAL IMPLICATIONS: In addition to inciting pleural inflammation essential for pleural fibrosis, IL6, IL8, G-CSF, sVCAM and CD40-Ligand could account for the additional effect of apoptosis of lung adenocarcinoma cells.

DISCLOSURE: Pyng Lee, No Financial Disclosure Information; No Product/Research Disclosure Information

12:45 PM - 2:00 PM




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