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In vivo induction of apoptosis by fucoxanthin, a marine carotenoid, associated with down-regulating STAT3/EGFR signaling in sarcoma 180 (S180) xenografts-bearing mice.

Wang J, Chen S, Xu S, Yu X, Ma D, Hu X, Cao X - Mar Drugs (2012)

Bottom Line: But the precise mechanism by which fucoxanthin exerts anticarcinogenic effects is not yet fully understood.In addition, immunohistochemistry analysis and Western blotting analysis showed that fucoxanthin significantly decreased the expressions of survivin and vascular endothelial growth factor (VEGF).Most importantly, fucoxanthin inhibited the expressions of the epidermal growth factor receptor (EGFR) and STAT3 and phosphorylated STAT3 proteins.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, College of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China. wangj79@hotmail.com

ABSTRACT
Previous in vitro researches have showed that fucoxanthin, a natural carotenoid isolated from sargassum, can inhibit proliferation or induce apoptosis in human neuroblastoma, hepatoma, leukemia, colon carcinoma, prostate cancer or urinary bladder cancer cells. But the precise mechanism by which fucoxanthin exerts anticarcinogenic effects is not yet fully understood. In this study, we performed an in vivo study to investigate the anti-tumor effect and mechanisms of fucoxanthin on xenografted sarcoma 180 (S180) in mice. Results revealed that fucoxanthin significantly inhibited the growth of sarcoma at the dose of 50 or 100 mg/kg. TUNEL analysis showed that the number of positive cells in the fucoxanthin-treated group was higher than that in the control group. Western blotting analysis also revealed the suppressed expression of bcl-2 and enhanced expression of cleaved caspase-3 by fucoxanthin. In addition, immunohistochemistry analysis and Western blotting analysis showed that fucoxanthin significantly decreased the expressions of survivin and vascular endothelial growth factor (VEGF). Most importantly, fucoxanthin inhibited the expressions of the epidermal growth factor receptor (EGFR) and STAT3 and phosphorylated STAT3 proteins. These results indicated that in vivo induction of apoptosis by fucoxanthin is associated with down-regulating STAT3/EGFR signaling in S180 xenografts-bearing mice.

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TUNEL analysis for the apoptosis in S180 sarcoma tissue. These sarcoma sections were obtained from the following pretreatment and treatment groups: soybean oil (control), sarcoma 180 (CTX) (20 mg/kg), fucoxanthin at doses of 25 mg/kg, 50 mg/kg and 100 mg/kg. TUNEL-Labeled sarcoma sections showed, following treatment with fucoxanthin (50, 100 mg/kg) and CTX, TUNEL-positive apoptotic cells with brown nuclear staining (black arrow) are significantly greater than those in control (×200). Slides are representative of 15 animals per group.
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marinedrugs-10-02055-f001: TUNEL analysis for the apoptosis in S180 sarcoma tissue. These sarcoma sections were obtained from the following pretreatment and treatment groups: soybean oil (control), sarcoma 180 (CTX) (20 mg/kg), fucoxanthin at doses of 25 mg/kg, 50 mg/kg and 100 mg/kg. TUNEL-Labeled sarcoma sections showed, following treatment with fucoxanthin (50, 100 mg/kg) and CTX, TUNEL-positive apoptotic cells with brown nuclear staining (black arrow) are significantly greater than those in control (×200). Slides are representative of 15 animals per group.

Mentions: Apoptosis in sarcoma was detected by in situ end-labeling of nuclear DNA fragments (TUNEL) staining. In the TUNEL assay (Figure 1), sarcoma sections from the model control group showed only slight background stained with a few TUNEL-positive cells (5.29 ± 0.28 apoptotic cells/×200 field), whereas in the CTX-treated group, the number of TUNEL-positive cells significantly increased (16.29 ± 0.68 apoptotic cells/×200 field, p < 0.01, vs. model control group). Following treatment with fucoxanthin (50 and 100 mg/kg), the number of TUNEL-positive cells also markedly elevated (9.03 ± 0.58 apoptotic cells/×200 field in 50 mg/kg fucoxanthin group; 17.53 ± 0.62 apoptotic cells/×200 field in 100 mg/kg fucoxanthin group, p < 0.05 or p < 0.01, vs. model control group).


In vivo induction of apoptosis by fucoxanthin, a marine carotenoid, associated with down-regulating STAT3/EGFR signaling in sarcoma 180 (S180) xenografts-bearing mice.

Wang J, Chen S, Xu S, Yu X, Ma D, Hu X, Cao X - Mar Drugs (2012)

TUNEL analysis for the apoptosis in S180 sarcoma tissue. These sarcoma sections were obtained from the following pretreatment and treatment groups: soybean oil (control), sarcoma 180 (CTX) (20 mg/kg), fucoxanthin at doses of 25 mg/kg, 50 mg/kg and 100 mg/kg. TUNEL-Labeled sarcoma sections showed, following treatment with fucoxanthin (50, 100 mg/kg) and CTX, TUNEL-positive apoptotic cells with brown nuclear staining (black arrow) are significantly greater than those in control (×200). Slides are representative of 15 animals per group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3475273&req=5

marinedrugs-10-02055-f001: TUNEL analysis for the apoptosis in S180 sarcoma tissue. These sarcoma sections were obtained from the following pretreatment and treatment groups: soybean oil (control), sarcoma 180 (CTX) (20 mg/kg), fucoxanthin at doses of 25 mg/kg, 50 mg/kg and 100 mg/kg. TUNEL-Labeled sarcoma sections showed, following treatment with fucoxanthin (50, 100 mg/kg) and CTX, TUNEL-positive apoptotic cells with brown nuclear staining (black arrow) are significantly greater than those in control (×200). Slides are representative of 15 animals per group.
Mentions: Apoptosis in sarcoma was detected by in situ end-labeling of nuclear DNA fragments (TUNEL) staining. In the TUNEL assay (Figure 1), sarcoma sections from the model control group showed only slight background stained with a few TUNEL-positive cells (5.29 ± 0.28 apoptotic cells/×200 field), whereas in the CTX-treated group, the number of TUNEL-positive cells significantly increased (16.29 ± 0.68 apoptotic cells/×200 field, p < 0.01, vs. model control group). Following treatment with fucoxanthin (50 and 100 mg/kg), the number of TUNEL-positive cells also markedly elevated (9.03 ± 0.58 apoptotic cells/×200 field in 50 mg/kg fucoxanthin group; 17.53 ± 0.62 apoptotic cells/×200 field in 100 mg/kg fucoxanthin group, p < 0.05 or p < 0.01, vs. model control group).

Bottom Line: But the precise mechanism by which fucoxanthin exerts anticarcinogenic effects is not yet fully understood.In addition, immunohistochemistry analysis and Western blotting analysis showed that fucoxanthin significantly decreased the expressions of survivin and vascular endothelial growth factor (VEGF).Most importantly, fucoxanthin inhibited the expressions of the epidermal growth factor receptor (EGFR) and STAT3 and phosphorylated STAT3 proteins.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, College of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China. wangj79@hotmail.com

ABSTRACT
Previous in vitro researches have showed that fucoxanthin, a natural carotenoid isolated from sargassum, can inhibit proliferation or induce apoptosis in human neuroblastoma, hepatoma, leukemia, colon carcinoma, prostate cancer or urinary bladder cancer cells. But the precise mechanism by which fucoxanthin exerts anticarcinogenic effects is not yet fully understood. In this study, we performed an in vivo study to investigate the anti-tumor effect and mechanisms of fucoxanthin on xenografted sarcoma 180 (S180) in mice. Results revealed that fucoxanthin significantly inhibited the growth of sarcoma at the dose of 50 or 100 mg/kg. TUNEL analysis showed that the number of positive cells in the fucoxanthin-treated group was higher than that in the control group. Western blotting analysis also revealed the suppressed expression of bcl-2 and enhanced expression of cleaved caspase-3 by fucoxanthin. In addition, immunohistochemistry analysis and Western blotting analysis showed that fucoxanthin significantly decreased the expressions of survivin and vascular endothelial growth factor (VEGF). Most importantly, fucoxanthin inhibited the expressions of the epidermal growth factor receptor (EGFR) and STAT3 and phosphorylated STAT3 proteins. These results indicated that in vivo induction of apoptosis by fucoxanthin is associated with down-regulating STAT3/EGFR signaling in S180 xenografts-bearing mice.

Show MeSH
Related in: MedlinePlus