Background: Apigenin, a common edible plant flavonoid, is a well characterised antioxidant.The adipokine leptin exerts proliferative and anti-apoptotic activities in a variety ofcell types. In cancer cells, apigenin may induce a pro-apoptotic pathway whereas leptinhas an anti-apoptotic role. The purpose of the study is to investigate the role of apigeninand of leptin/leptin receptor pathway on proliferation and on apoptosis in lung adenocarcinoma.Methods: Immunocytochemistry, flow cytometry and RT-q-RT PCR, were used to investigatethe expression and modulation of leptin receptors on the lung adenocarcinoma cell lineA549 in presence or absence of apigenin and of leptin, alone or combined. Clonogenic testto evaluate cell proliferation was assessed. Exogenous leptin binding to its receptors by flowcytometry, reactive oxygen species (ROS) by dichlorofluorescein diacetate analysis, celldeath by ethidium bromide and apoptosis by annexin V analysis were assessed. Apoptosiswas assessed also in presence of lung adenocarcinoma pleural fluids (PF) (n = 6).Results: A549 express leptin/leptin receptor pathway and its expression is upregulated byapigenin. Apigenin alone or combined with leptin significantly decreases cell proliferationand significantly increases the spontaneous release of ROS, with augmented cell death andapoptosis, this latter also in the presence of lung adenocarcinoma PF. Leptin alone significantlyincreases cell proliferation and significantly decreases cell death.Conclusions: These results strongly suggest the potential utility of the flavonoid apigenin inthe complementary therapeutic approach of patients with lung adenocarcinoma.
|Number of pages||10|
|Journal||European Journal of Cancer|
|Publication status||Published - 2011|
All Science Journal Classification (ASJC) codes
- Cancer Research