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Mastic oil inhibits the metastatic phenotype of mouse lung adenocarcinoma cells.

Loutrari H, Magkouta S, Papapetropoulos A, Roussos C - Cancers (Basel) (2011)

Bottom Line: However, no studies have addressed its anti-metastatic actions.Moreover, exposure of LLC and endothelial cells to mastic oil impaired their adhesive interactions in a co-culture assay and reduced the expression of key adhesion molecules by endothelial cells upon their stimulation with tumor necrosis factor-alpha.Overall, this study provides novel evidence supporting a multipotent role for mastic oil in prevention of crucial processes related to cancer metastasis.

View Article: PubMed Central - PubMed

Affiliation: "G.P. Livanos and M. Simou Laboratories", Evangelismos Hospital, Department of Critical Care and Pulmonary Services, School of Medicine, University of Athens, 3 Ploutarchou Street, 10675 Athens, Greece. elloutrar@med.uoa.gr.

ABSTRACT
Mastic oil from Pistacia lentiscus variation chia, a natural combination of bioactive terpenes, has been shown to exert anti-tumor growth effects against a broad spectrum of cancers including mouse Lewis lung adenocarcinomas (LLC). However, no studies have addressed its anti-metastatic actions. In this study, we showed that treatment of LLC cells with mastic oil within a range of non-toxic concentrations (0.01-0.04% v/v): (a) abrogated their Matrigel invasion and migration capabilities in transwell assays; (b) reduced the levels of secreted MMP-2; (c) restricted phorbol ester-induced actin remodeling and (d) limited the length of neo-vessel networks in tumor microenvironment in the model of chick embryo chorioallantoic membrane. Moreover, exposure of LLC and endothelial cells to mastic oil impaired their adhesive interactions in a co-culture assay and reduced the expression of key adhesion molecules by endothelial cells upon their stimulation with tumor necrosis factor-alpha. Overall, this study provides novel evidence supporting a multipotent role for mastic oil in prevention of crucial processes related to cancer metastasis.

No MeSH data available.


Related in: MedlinePlus

Mastic oil inhibits actin polymerization in PMA-induced LLC cells. Serum-starved LLC cells were treated with Moil (0.04% v/v), POH (1.0 mM) or vehicle (CTL) for 3 h and then induced by 1 μM PMA or vehicle (basal) for 30 min. Cells were fixed and F-actin was visualized by phalloidin staining. Top panel: representative micro-photographs (630 X magnification); bottom panel: graphs from image analysis of F-actin staining normalized to cell numbers and expressed as mean (% of control) ± SEM; n = 96–160, *P < 0.05.
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f2-cancers-03-00789: Mastic oil inhibits actin polymerization in PMA-induced LLC cells. Serum-starved LLC cells were treated with Moil (0.04% v/v), POH (1.0 mM) or vehicle (CTL) for 3 h and then induced by 1 μM PMA or vehicle (basal) for 30 min. Cells were fixed and F-actin was visualized by phalloidin staining. Top panel: representative micro-photographs (630 X magnification); bottom panel: graphs from image analysis of F-actin staining normalized to cell numbers and expressed as mean (% of control) ± SEM; n = 96–160, *P < 0.05.

Mentions: It has been well established that the process of cell motility requires the dynamic organization of the actin cytoskeleton, which in turn involves the polymerization and depolymerization of actin filaments in response to chemotactic stimuli [32]. Therefore, to explore the basis of mastic oil-mediated inhibitory action on LLC cell motility, we subsequently investigated its potential effects on actin cytoskeleton remodeling using phorbol 12-myristate 13-acetate (PMA) as inducer, a tumor promoter signaling phospholipid [33]. Actin rearrangement in mastic oil (0.01–0.04 % v/v), POH (0.5–1.0 mM) or vehicle treated LLC cells was assessed before and after addition of PMA by means of immunofluorescent labeling and confocal microscopy of filamentous (F)-actin. As shown in Figure 2 (which illustrates the effects in the high concentration range), although non-induced LLC cells displayed low basal levels of polymerized F-actin, exposure to PMA caused a prominent staining especially at the periphery, indicating an increase in de novo actin polymerization. Importantly, pre-incubation with mastic oil and POH resulted in a significant attenuation of F-actin fiber formation in PMA-stimulated cells thus suggesting the ability of these agents to attenuate pathways triggering changes in the actin cytoskeleton such as those induced by the used phospholipid [32-34].


Mastic oil inhibits the metastatic phenotype of mouse lung adenocarcinoma cells.

Loutrari H, Magkouta S, Papapetropoulos A, Roussos C - Cancers (Basel) (2011)

Mastic oil inhibits actin polymerization in PMA-induced LLC cells. Serum-starved LLC cells were treated with Moil (0.04% v/v), POH (1.0 mM) or vehicle (CTL) for 3 h and then induced by 1 μM PMA or vehicle (basal) for 30 min. Cells were fixed and F-actin was visualized by phalloidin staining. Top panel: representative micro-photographs (630 X magnification); bottom panel: graphs from image analysis of F-actin staining normalized to cell numbers and expressed as mean (% of control) ± SEM; n = 96–160, *P < 0.05.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3756390&req=5

f2-cancers-03-00789: Mastic oil inhibits actin polymerization in PMA-induced LLC cells. Serum-starved LLC cells were treated with Moil (0.04% v/v), POH (1.0 mM) or vehicle (CTL) for 3 h and then induced by 1 μM PMA or vehicle (basal) for 30 min. Cells were fixed and F-actin was visualized by phalloidin staining. Top panel: representative micro-photographs (630 X magnification); bottom panel: graphs from image analysis of F-actin staining normalized to cell numbers and expressed as mean (% of control) ± SEM; n = 96–160, *P < 0.05.
Mentions: It has been well established that the process of cell motility requires the dynamic organization of the actin cytoskeleton, which in turn involves the polymerization and depolymerization of actin filaments in response to chemotactic stimuli [32]. Therefore, to explore the basis of mastic oil-mediated inhibitory action on LLC cell motility, we subsequently investigated its potential effects on actin cytoskeleton remodeling using phorbol 12-myristate 13-acetate (PMA) as inducer, a tumor promoter signaling phospholipid [33]. Actin rearrangement in mastic oil (0.01–0.04 % v/v), POH (0.5–1.0 mM) or vehicle treated LLC cells was assessed before and after addition of PMA by means of immunofluorescent labeling and confocal microscopy of filamentous (F)-actin. As shown in Figure 2 (which illustrates the effects in the high concentration range), although non-induced LLC cells displayed low basal levels of polymerized F-actin, exposure to PMA caused a prominent staining especially at the periphery, indicating an increase in de novo actin polymerization. Importantly, pre-incubation with mastic oil and POH resulted in a significant attenuation of F-actin fiber formation in PMA-stimulated cells thus suggesting the ability of these agents to attenuate pathways triggering changes in the actin cytoskeleton such as those induced by the used phospholipid [32-34].

Bottom Line: However, no studies have addressed its anti-metastatic actions.Moreover, exposure of LLC and endothelial cells to mastic oil impaired their adhesive interactions in a co-culture assay and reduced the expression of key adhesion molecules by endothelial cells upon their stimulation with tumor necrosis factor-alpha.Overall, this study provides novel evidence supporting a multipotent role for mastic oil in prevention of crucial processes related to cancer metastasis.

View Article: PubMed Central - PubMed

Affiliation: "G.P. Livanos and M. Simou Laboratories", Evangelismos Hospital, Department of Critical Care and Pulmonary Services, School of Medicine, University of Athens, 3 Ploutarchou Street, 10675 Athens, Greece. elloutrar@med.uoa.gr.

ABSTRACT
Mastic oil from Pistacia lentiscus variation chia, a natural combination of bioactive terpenes, has been shown to exert anti-tumor growth effects against a broad spectrum of cancers including mouse Lewis lung adenocarcinomas (LLC). However, no studies have addressed its anti-metastatic actions. In this study, we showed that treatment of LLC cells with mastic oil within a range of non-toxic concentrations (0.01-0.04% v/v): (a) abrogated their Matrigel invasion and migration capabilities in transwell assays; (b) reduced the levels of secreted MMP-2; (c) restricted phorbol ester-induced actin remodeling and (d) limited the length of neo-vessel networks in tumor microenvironment in the model of chick embryo chorioallantoic membrane. Moreover, exposure of LLC and endothelial cells to mastic oil impaired their adhesive interactions in a co-culture assay and reduced the expression of key adhesion molecules by endothelial cells upon their stimulation with tumor necrosis factor-alpha. Overall, this study provides novel evidence supporting a multipotent role for mastic oil in prevention of crucial processes related to cancer metastasis.

No MeSH data available.


Related in: MedlinePlus