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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 effects on tumor cell invasion/migration and MMP expression. (A) Mastic oil attenuates tumor cell invasion and migration. Serum starved LLC cells were treated with Moil (0.01–0.02% v/v), POH (0.5mM) or vehicle (CTL) for 2 h and then loaded onto BD Matrigel Invasion or Control chambers. The lower chambers were filled with complete medium containing test agents and plates were incubated for 20 h. Migrating cells were counted (200 X magnification, 10 HPF/membrane) and results are expressed as mean ± SEM; n = 9, *P < 0.05 from vehicle. (B) Mastic oil effects on MMP-2 and MMP-9 expression. Serum starved LLC cultures were treated with Moil (0.02–0.04 % v/v), POH (1 mM) or vehicle (CTL) for 48 h and supernatants were analyzed for MMP-2 and MMP-9 levels by ELISA. Results were normalized to total protein and are expressed as mean ± SEM; n = 12, *P < 0.05 from vehicle.
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f1-cancers-03-00789: Mastic oil effects on tumor cell invasion/migration and MMP expression. (A) Mastic oil attenuates tumor cell invasion and migration. Serum starved LLC cells were treated with Moil (0.01–0.02% v/v), POH (0.5mM) or vehicle (CTL) for 2 h and then loaded onto BD Matrigel Invasion or Control chambers. The lower chambers were filled with complete medium containing test agents and plates were incubated for 20 h. Migrating cells were counted (200 X magnification, 10 HPF/membrane) and results are expressed as mean ± SEM; n = 9, *P < 0.05 from vehicle. (B) Mastic oil effects on MMP-2 and MMP-9 expression. Serum starved LLC cultures were treated with Moil (0.02–0.04 % v/v), POH (1 mM) or vehicle (CTL) for 48 h and supernatants were analyzed for MMP-2 and MMP-9 levels by ELISA. Results were normalized to total protein and are expressed as mean ± SEM; n = 12, *P < 0.05 from vehicle.

Mentions: Since invasion of the extracellular matrix (ECM) by cancer cells is essential for their dissemination, we first examined in a transwell in vitro assay the capability of mastic oil-treated tumor cells to invade and move through Matrigel-coated filters. Migration of tumor cells through identical uncoated membranes was also assessed in parallel using similar experimental conditions. As shown in Figure 1A, mastic oil even at low concentrations (0.01% and 0.02% v/v) significantly limited tumor cell invasiveness and migration capabilities indicating that it could target both the enzymatic machinery involved in ECM degradation and the cell motility mechanism [28]. Notably, POH at 0.5 mM (Figure 1A) and 1.0 mM (not shown) although affecting LLC cell migration, was not able to cause any significant change in the number of invading LLC cells, thus underlining the contribution of additional bioactive ingredients into mastic oil.


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

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

Mastic oil effects on tumor cell invasion/migration and MMP expression. (A) Mastic oil attenuates tumor cell invasion and migration. Serum starved LLC cells were treated with Moil (0.01–0.02% v/v), POH (0.5mM) or vehicle (CTL) for 2 h and then loaded onto BD Matrigel Invasion or Control chambers. The lower chambers were filled with complete medium containing test agents and plates were incubated for 20 h. Migrating cells were counted (200 X magnification, 10 HPF/membrane) and results are expressed as mean ± SEM; n = 9, *P < 0.05 from vehicle. (B) Mastic oil effects on MMP-2 and MMP-9 expression. Serum starved LLC cultures were treated with Moil (0.02–0.04 % v/v), POH (1 mM) or vehicle (CTL) for 48 h and supernatants were analyzed for MMP-2 and MMP-9 levels by ELISA. Results were normalized to total protein and are expressed as mean ± SEM; n = 12, *P < 0.05 from vehicle.
© Copyright Policy
Related In: Results  -  Collection

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

f1-cancers-03-00789: Mastic oil effects on tumor cell invasion/migration and MMP expression. (A) Mastic oil attenuates tumor cell invasion and migration. Serum starved LLC cells were treated with Moil (0.01–0.02% v/v), POH (0.5mM) or vehicle (CTL) for 2 h and then loaded onto BD Matrigel Invasion or Control chambers. The lower chambers were filled with complete medium containing test agents and plates were incubated for 20 h. Migrating cells were counted (200 X magnification, 10 HPF/membrane) and results are expressed as mean ± SEM; n = 9, *P < 0.05 from vehicle. (B) Mastic oil effects on MMP-2 and MMP-9 expression. Serum starved LLC cultures were treated with Moil (0.02–0.04 % v/v), POH (1 mM) or vehicle (CTL) for 48 h and supernatants were analyzed for MMP-2 and MMP-9 levels by ELISA. Results were normalized to total protein and are expressed as mean ± SEM; n = 12, *P < 0.05 from vehicle.
Mentions: Since invasion of the extracellular matrix (ECM) by cancer cells is essential for their dissemination, we first examined in a transwell in vitro assay the capability of mastic oil-treated tumor cells to invade and move through Matrigel-coated filters. Migration of tumor cells through identical uncoated membranes was also assessed in parallel using similar experimental conditions. As shown in Figure 1A, mastic oil even at low concentrations (0.01% and 0.02% v/v) significantly limited tumor cell invasiveness and migration capabilities indicating that it could target both the enzymatic machinery involved in ECM degradation and the cell motility mechanism [28]. Notably, POH at 0.5 mM (Figure 1A) and 1.0 mM (not shown) although affecting LLC cell migration, was not able to cause any significant change in the number of invading LLC cells, thus underlining the contribution of additional bioactive ingredients into mastic oil.

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