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Biological Effects of Rosemary Extract in Human Lung Cancer Cells
Author(s) -
Moore Jessy,
Naimi Madina,
Tsiani Evangelia
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb141
Subject(s) - clonogenic assay , cell growth , lung cancer , a549 cell , protein kinase b , pi3k/akt/mtor pathway , cancer research , cell , cell culture , cancer cell , medicine , cancer , signal transduction , biology , chemistry , pharmacology , microbiology and biotechnology , biochemistry , genetics
Lung cancer accounts for the most cancer‐related deaths. Non‐small cell lung cancer (NSCLC) represents a very aggressive form of lung cancer and is characterized by resistance to chemo‐ and radiotherapy thus, finding new ways to inhibit NSCLC cell proliferation and survival is very important. Many phytochemicals have emerged as having potential chemotherapeutic effects and rosemary extract (RE) has been shown to have anticancer properties in vitro and in vivo however, limited evidence exists regarding its effect in NSCLC cells. The objectives of the present study were to examine the effects of RE on NSCLC cell proliferation, and investigate its effects on the phosphatidylinositol 3‐kinase (PI3K)‐Akt and AMP‐activated protein kinase (AMPK) signaling pathways which regulate cell proliferation and survival. Various NSCLC cell lines (A549, H1299, H460) with different histologies and mutations were treated with varying concentrations of RE. Cell proliferation was measured by crystal violet assay, clonogenic assays were performed to examine the effects of RE on cell survival, and immunoblotting with phospho‐ specific antibodies was performed to examine signaling events. RE dose‐dependently inhibited cell proliferation in all cell lines. Significant inhibition of cell proliferation was seen at concentrations as low as 5µg/mL. Maximum inhibition (% of untreated control ± SE) was seen at 50µg/mL (21.9% ± 2.6, p<0.001) in A549, 50µg/mL (30.7% ± 3.0, p<0.001) in H460, and 25µg/mL (23.3% ± 1.3, p<0.001) in H1299 cells. RE (50µg/mL) inhibited total and phosphorylated levels of Akt, while phosphorylated levels of AMPK were enhanced. Clonogenic survival was also inhibited by RE. Our data suggest that RE may have potent anticancer properties in NSCLC and warrants further investigation.