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Molecules
2016 May 12;215:. doi: 10.3390/molecules21050625.
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In Vivo Anti-Cancer Mechanism of Low-Molecular-Weight Fucosylated Chondroitin Sulfate (LFCS) from Sea Cucumber Cucumaria frondosa.
Liu X
,
Liu Y
,
Hao J
,
Zhao X
,
Lang Y
,
Fan F
,
Cai C
,
Li G
,
Zhang L
,
Yu G
.
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The low-molecular-weight fucosylated chondroitin sulfate (LFCS) was prepared from native fucosylated chondroitin sulfate (FCS), which was extracted and isolated from sea cucumber Cucumaria frondosa, and the anti-cancer mechanism of LFCS on mouse Lewis lung carcinoma (LLC) was investigated. The results showed that LFCS remarkably inhibited LLC growth and metastasis in a dose-dependent manner. LFCS induced cell cycle arrest by increasing p53/p21 expression and apoptosis through activation of caspase-3 activity in LLC cells. Meanwhile, LFCS suppressed the expression of vascular endothelial growth factor (VEGF), increased the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) and downregulated the matrix metalloproteinases (MMPs) level. Furthermore, LFCS significantly suppressed the activation of ERK1/2/p38 MAPK/NF-κB pathway, which played a prime role in expression of MMPs. All of these data indicate LFCS may be used as anti-cancer drug candidates and deserve further study.
Figure 5. LFCS increased protein expression of p53, p21, and caspase-3 in LLC cells after 72 h treatment of LFCS detected by Western blot. Expression of the β-actin was used as internal control. Lane 1: vehicle-treated cells; Lane 2: 50 μg/mL LFCS-treated cells; Lane 3: 400 μg/mL LFCS-treated cells. Data were presented as mean ± SD and derived from one representative experiment performed in triplicate. * p < 0.05, ** p < 0.01, significant difference compared with control group.
Figure 6. LFCS suppressed metastasis and angiogenesis by regulating protein expression of MMP-9, TIMP-1, VEGF, p38, ERK1/2, and NF-κB in LLC cells after 72 h treatment of LFCS detected by Western blot. (A) LFCS increased TIMP-1, and decreased MMP-9 and VEGF expression; (B) LFCS suppressed NF-κB, p38 and ERK1/2 expression. Expression of the β-actin was used as internal control. Lane 1: vehicle-treated cells; Lane 2: 50 μg/mL LFCS-treated cells; Lane 3: 400 μg/mL LFCS-treated cells. Data were presented as mean ± SD and derived from one representative experiment performed in triplicate. * p < 0.05, ** p < 0.01, significant difference compared with control group.
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