Fluorescent Labeling of Polymannuronic Acid and Its Distribution in Mice by Tail Vein Injection.

Polymannuronic acid (PM) possesses more pharmacological activities than sodium alginate, but there have been few studies on its absorption mechanism, tissue distribution, and pharmacokinetics. Studies of pharmacokinetics and tissue distribution are necessary to elucidate the pharmacological effects of PM. Thus, we used fluorescein isothiocyanate (FITC) to produce fluorescently labeled PM (FITC-PM) and detected the distribution and pharmacokinetics of PM in vivo via tail vein injection. The results demonstrate that the FITC-PM showed high stability in different pH solutions. After the tail vein injection, FITC-PM tended to be distributed in the kidney, followed by the liver and in the heart, spleen, and lungs at lower concentrations. Pharmacokinetic analysis showed that the elimination rate constant of FITC-PM was 0.24, the half-life time was 2.85 h, the peak concentration was 235.17 µg/mL, the area under the curve was 631.48 µg/mL·h, the area under the curve by statistical moment was 1843.15 µg/mL·h2, the mean residence time was 2.92 h, and the clearance rate was 79.18 mL/h. These results indicate that FITC-PM could be used for PM distribution and pharmacokinetic studies, and the studies of pharmacokinetics and tissue distribution provided basic information that can be used to further clarify PM pharmacodynamic mechanisms.

Current Research Landscape of Marine-Derived Anti-Atherosclerotic Substances.

Atherosclerosis is a chronic disease characterized by lipid accumulation and chronic inflammation of the arterial wall, which is the pathological basis for coronary heart disease, cerebrovascular disease and thromboembolic disease. Currently, there is a lack of low-cost therapeutic agents that effectively slow the progression of atherosclerosis. Therefore, the development of new drugs is urgently needed. The research and development of marine-derived drugs have gained increasing interest from researchers across the world. Many marine organisms provide a rich material basis for the development of atherosclerotic drugs. This review focuses on the latest technological advances in the structures and mechanisms of action of marine-derived anti-atherosclerotic substances and the challenges of the application of these substances including marine polysaccharides, proteins and peptides, polyunsaturated fatty acids and small molecule compounds. Here, we describe the theoretical basis of marine biological resources in the treatment of atherosclerosis.

Advances in the Study of Marine Products with Lipid-Lowering Properties.

With twice the number of cancer's deaths, cardiovascular diseases have become the leading cause of death worldwide. Atherosclerosis, in particular, is a progressive, chronic inflammatory cardiovascular disease caused by persistent damage to blood vessels due to elevated cholesterol levels and hyperlipidemia. This condition is characterized by an increase in serum cholesterol, triglycerides, and low-density lipoprotein, and a decrease in high-density lipoprotein. Although existing therapies with hypolipidemic effects can improve the living standards of patients with cardiovascular diseases, the drugs currently used in clinical practice have certain side effects, which insists on the need for the development of new types of drugs with lipid-lowering effects. Some marine-derived substances have proven hypolipidemic activities with fewer side effects and stand as a good alternative for drug development. Recently, there have been thousands of studies on substances with lipid-lowering properties of marine origin, and some are already implemented in clinical practice. Here, we summarize the active components of marine-derived products having a hypolipidemic effect. These active constituents according to their source are divided into algal, animal, plant and microbial and contribute to the development and utilization of marine medicinal products with hypolipidemic effects.

Fucoidan Induces Apoptosis of HT-29 Cells via the Activation of DR4 and Mitochondrial Pathway.

Fucoidan has a variety of pharmacological activities, but the understanding of the mechanism of fucoidan-induced apoptosis of colorectal cancer cells remains limited. The results of the present study demonstrated that the JNK signaling pathway is involved in the activation of apoptosis in colorectal cancer-derived HT-29 cells, and fucoidan induces apoptosis by activation of the DR4 at the transcriptional and protein levels. The survival rate of HT-29 cells was approximately 40% in the presence of 800 µg/mL of fucoidan, but was increased to 70% after DR4 was silenced by siRNA. Additionally, fucoidan has been shown to reduce the mitochondrial membrane potential and destroy the integrity of mitochondrial membrane. In the presence of an inhibitor of cytochrome C inhibitor and DR4 siRNA or the presence of cytochrome C inhibitor only, the cell survival rate was significantly higher than when cells were treated with DR4 siRNA only. These data indicate that both the DR4 and the mitochondrial pathways contribute to fucoidan-induced apoptosis of HT-29 cells, and the extrinsic pathway is upstream of the intrinsic pathway. In conclusion, the current work identified the mechanism of fucoidan-induced apoptosis and provided a novel theoretical basis for the future development of clinical applications of fucoidan as a drug.

Advances in Research on the Bioactivity of Alginate Oligosaccharides.

Alginate is a natural polysaccharide present in various marine brown seaweeds. Alginate oligosaccharide (AOS) is a degradation product of alginate, which has received increasing attention due to its low molecular weight and promising biological activity. The wide-ranging biological activity of AOS is closely related to the diversity of their structures. AOS with a specific structure and distinct applications can be obtained by different methods of alginate degradation. This review focuses on recent advances in the biological activity of alginate and its derivatives, including their anti-tumor, anti-oxidative, immunoregulatory, anti-inflammatory, neuroprotective, antibacterial, hypolipidemic, antihypertensive, and hypoglycemic properties, as well as the ability to suppress obesity and promote cell proliferation and regulate plant growth. We hope that this review will provide theoretical basis and inspiration for the high-value research developments and utilization of AOS-related products.

Advances in Studies on the Pharmacological Activities of Fucoxanthin.

Fucoxanthin is a natural carotenoid derived mostly from many species of marine brown algae. It is characterized by small molecular weight, is chemically active, can be easily oxidized, and has diverse biological activities, thus protecting cell components from ROS. Fucoxanthin inhibits the proliferation of a variety of cancer cells, promotes weight loss, acts as an antioxidant and anti-inflammatory agent, interacts with the intestinal flora to protect intestinal health, prevents organ fibrosis, and exerts a multitude of other beneficial effects. Thus, fucoxanthin has a wide range of applications and broad prospects. This review focuses primarily on the latest progress in research on its pharmacological activity and underlying mechanisms.

Study on Absorption Mechanism and Tissue Distribution of Fucoidan.

Fucoidan exhibits several pharmacological activities and is characterized by high safety and the absence of toxic side effects. However, the absorption of fucoidan is not well-characterized. In the present study, fucoidan were labeled with fluorescein isothiocyanate (FITC) and their ability to traverse a monolayer of Caco-2 cells was examined. The apparent permeability coefficients (Papp × 10-6) of FITC-labeled fucoidan (FITC-fucoidan) were 26.23, 20.15, 17.93, 16.11 cm/sec, respectively, at the concentration of 10 µg/mL at 0.5, 1, 1.5 and 2 h. The absorption of FITC-fucoidan was suppressed by inhibitors of clathrin-mediated endocytosis, chlorpromazine, NH4Cl, and Dynasore; the inhibition rates were 84.24%, 74.61%, and 63.94%, respectively. This finding suggested that clathrin-mediated endocytosis was involved in fucoidan transport. Finally, tissue distribution of FITC-fucoidan was studied in vivo after injection of 50 mg/kg body weight into the tail vein of mice. The results showed that FITC-fucoidan targeted kidney and liver, reaching concentrations of 1092.31 and 284.27 µg/g respectively after 0.5 h. In summary, the present work identified the mechanism of absorption of fucoidan and documented its tissue distribution, providing a theoretical basis for the future development of fucoidan applications.

Determination of fucoidan in rat plasma by HPLC and its application in pharmacokinetics.

This is a new expanded method of determining the characterisation of fucoidan from Laminaria japonica (kelp) in rat plasma by high-performance liquid chromatography (HPLC) with fluorescence detection. We tagged fucoidan by fluoresce in isothiocyanate (FITC) for tracking and treated the plasma samples via protein precipitation with 10% trichloroacetic acid and methanol. Column chromatography separation was on a TSK-G4000sw column (7.8 mm × 300 mm, 5 mm) by elution with 0.15 M NaCl. The quantification of fucoidan was performed by HPLC with fluorescence detection. The results suggested that the calibration curve for fucoidan concentration was linear dependent in the limits of 0.5-100µg/mL. The lower limit of quantitation (LLOQ) was 0.5µg/mL and the lower limit of detection (LLOD) was 0.15µg/mL. The intra-day and inter-day precision values were less than 13%and the accuracy ranged from 96.83 to 100.03% at 3 different concentrations. The fucoidan stability of rat plasma at different temperatures and time-points was estimated. The extraction efficiencies ranged from 93.33 to 96.53%and the matrix effect ranged from 92.67 to 95.83%. Method selectivity was evaluated as well. We successfully studied the pharmacokinetic of fucoidan in rat plasma after oral by the validated method. Fucoidan was administered to rats intravenously at a dose of 6 mg/kg and orally at a dose of 20 mg/kg. The Cmax was 7.33µg/mL within 2 h by oral administration; The initial Cmax was 75.59µg/mL. The bioavailability of fucoidan after oral administration to rats was 8.91%.

Biological Activities of Fucoidan and the Factors Mediating Its Therapeutic Effects: A Review of Recent Studies.

The marine acid polysaccharide fucoidan has attracted attention from both the food and pharmaceutical industries due to its promising therapeutic effects. Fucoidan is a polysaccharide that mainly consists of L-fucose and sulphate groups. Its excellent biological function is attributed to its unique biological structure. Classical activities include antitumor, antioxidant, anticoagulant, antithrombotic, immunoregulatory, antiviral and anti-inflammatory effects. More recently, fucoidan has been shown to alleviate metabolic syndrome, protect the gastrointestinal tract, benefit angiogenesis and bone health. This review focuses on the progress in our understanding of the biological activities of fucoidan, highlighting its benefits for the treatment of human disease. We hope that this review can provide some theoretical basis and inspiration for the product development of fucoidan.

The effect of leech extracts on endothelial cell coagulation-related factors and endothelial dysfuction-related molecules.

OBJECTIVE: This study was focused on screening leech extracts to identify those with little or no anti-coagulation effect or with significant anti-endothelial dysfunction activity. METHODS: Different leech extracts were prepared by enzymolysis and microbial transformation and their cytotoxicity were measured by MTT assay. The effect of different leech extracts on mRNA expression of coagulation-related factors (PAI, vWF, tPA, PS, TFPI, TM) was quantified by RT-PCR. After identifying a leech extract with little anti-coagulatory effect, RT-PCR was then used to assess the effect of this extract on the mRNA expression of endothelial dysfunction-related molecules (ET-1, iNOS, MCP-1, IL-6). RESULTS: 8 leech extracts were obtained, including 4 enzymatic extracts (LP, PHL, PTHL, CEHL) and 4 Lactobacillus metabolites (MRS, MRS-1, MRS-2, and MRS-3). Following optimization of conditions using MTT assays, we treated EA.hy926 cells with 0, 12.5, 25, 50 µg/mL of LP, PTHL, CEHL, MRS, MRS-1 or MRS-3 extract for 24 h. We found that PHL and MRS-1 had no significant effect on coagulation-related factors. Furthermore, treatment with 50 µg/mL PHL resulted in significant decreases in ET-1, iNOS, MCP-1, and IL-6 mRNA expression by 28.06%, 33.30%, 19.80%, and 52.34%, respectively. CONCLUSIONS: In the present study, we found that PHL, a pepsin hydrolysate of leech with little anti-coagulatory effect, could significantly suppress TNF-α induced mRNA overexpression of endothelial dysfunction-related molecules (ET-1, iNOS, MCP-1, and IL-6). These results provide a reliable experimental basis for identifying new anti-atherosclerosis therapeutics for long term use and with minimal bleeding side effects.

Characterization of a Novel PolyM-Preferred Alginate Lyase from Marine Vibrio splendidus OU02.

Alginate lyases are enzymes that degrade alginate into oligosaccharides which possess a variety of biological activities. Discovering and characterizing novel alginate lyases has great significance for industrial and medical applications. In this study, we reported a novel alginate lyase, AlyA-OU02, derived from the marine Vibrio splendidus OU02. The BLASTP searches showed that AlyA-OU02 belonged to polysaccharide lyase family 7 (PL7) and contained two consecutive PL7 domains, which was rare among the alginate lyases in PL7 family. Both the two domains, AlyAa and AlyAb, had lyase activities, while AlyAa exhibited polyM preference, and AlyAb was polyG-preferred. In addition, the enzyme activity of AlyAa was much higher than AlyAb at 25 °C. The full-length enzyme of AlyA-OU02 showed polyM preference, which was the same as AlyAa. AlyAa degraded alginate into di-, tri-, and tetra-alginate oligosaccharides, while AlyAb degraded alginate into tri-, tetra-, and penta-alginate oligosaccharides. The degraded products of AlyA-OU02 were similar to AlyAa. Our work provided a potential candidate in the application of alginate oligosaccharide production and the characterization of the two domains might provide insights into the use of alginate of this organism.

Use of fluorescein isothiocyanate isomer I to study the mechanism of intestinal absorption of fucoidan sulfate in vivo and in vitro.

A new method to label fucoidan sulfate was established with tyramine and fluorescein isothiocyanate isomer I (FITC). Fluorescence spectrophotometry and high performance liquid chromatography verified the successful labelling of fucoidan by FITC. The results of the single-pass intestinal perfusion indicated that the jejunum and ileum are the main absorption sites, and there was carrier saturation. In addition, fucoidan sulfate at 1 mg/ml had no inhibitory effect on Caco-2 cell proliferation. Studies on the transmembrane transport mechanism showed that fucoidan can be absorbed because the apparent permeability coefficient of the drugs (Papp ) A â†’ B was 3.78 + 0.03 ×10-6 and that of B â†’ A was 1.42 + 0.19 ×10-6 . The peak absorption of fucoidan occurred at 120 min after administration; moreover, the higher the concentration used, the worse the absorption was, suggesting the saturation of transport carriers. The absorption was temperature dependent: the absorption at 37°C was much better than that at 4°C. Further, the absorption of fucoidan sulfate might rely on clathrin endocytosis as chlorpromazine (10 µg/ml) significantly inhibited it.

Neuroprotective effect of sulfated polysaccharide isolated from sea cucumber Stichopus japonicus on 6-OHDA-induced death in SH-SY5Y through inhibition of MAPK and NF-κB and activation of PI3K/Akt signaling pathways.

The purpose of this study is to investigate the protective effect and molecular mechanism of the sulfated polysaccharide (SJP) isolated from the sea cucumber Stichopus japonicus against 6-OHDA-induced toxicity in SH-SY5Y cells. The results showed that SJP could protect SH-SY5Y cells against 6-OHDA-induced cell injury. We found that SJP effectively improves cell viability, decreases LDH leakage, and reverses morphological damage. Moreover, SJP significantly increases SOD activity but decreases MDA levels and ROS generation. Effect of SJP on 6-OHDA-induced cell death in SH-SY5Y cells is associated with an arrest in the G1/S phase of the cell cycle and inhibits the expression of Cyclin D3. 6-OHDA-induced intracellular generation of ROS and mitochondrial dysfunctions, release of cytochrome c, imbalance of Bax/Bcl-2, cleaved caspase-9/caspase-9 and cleaved caspase-3/caspase-3 ratio, and p-p53 activation were strikingly attenuated by SJP pretreatment. Meanwhile, SJP counteracted NF-κB activation, thereby preventing up-regulation of iNOS and intracellular NO release. The data provide the first evidence that SJP protects SH-SY5Y cells against 6-OHDA toxicity possibly by inhibiting MAPK and NF-κB and activating PI3K/Akt signaling pathways. Thus, SJP is a candidate for further evaluation of its protective effects against neurodegeneration in PD.

Icariin inhibits atherosclerosis progress in Apoe null mice by downregulating CX3CR1 in macrophage.

Horny Goat Weed is a commonly used in Chinese herbal medicine. And it is used in multiple kinds of diseases including cardiovascular diseases. Icariin is the major component isolated from Horny Goat Weed. It is reported to have lipid-lowering effect. In atherosclerosis, icariin attenuate the enhanced prothrombotic state independently of its lipid-lowering effects. However, its detail mechanism is remaining unclear. This study aimed to investigate the effect and mechanism of icariin on atherosclerosis. We performed gene expression profiling on icariin treated LPS-stimulated RAW264.7 and its control cells. Microarray analyses identified a list of genes significantly differentially expressed after icariin treated including downregulation of CX3CR1. Apoe null mice were assigned into 3 groups: control group, diet with 30 mg/kg/d icariin and diet with 60 mg/kg/d icariin. The results showed that icariin treatment significantly reduced lesion area and macrophage infiltration. Also icariin reduced CX3CR1 and CX3CL1 protein levels in the artery wall. In conclusion, icariin could be a potential anti-atherosclerosis agent by downregulating the expression of CX3CR1.

Stichopus japonicus Polysaccharide, Fucoidan, or Heparin Enhanced the SDF-1α/CXCR4 Axis and Promoted NSC Migration via Activation of the PI3K/Akt/FOXO3a Signaling Pathway.

Stichopus japonicus Polysaccharide (SJP) is a sulfated polysaccharide from the body wall of the sea cucumber, Stichopus japonicus. Fucoidan is a heparinoid compound that belongs to a family of sulfated polyfucose polysaccharides. Heparin is a glycosaminoglycan. SJP, fucoidan, and heparin profoundly promoted stromal cell-derived factor 1 alpha (SDF-1α)-induced neural stem cell (NSC) migration in a concentration-dependent manner. In addition, the basal migration capacity of cells was significantly promoted after incubation with SJP, fucoidan, or heparin. Interaction of SJP, fucoidan, or heparin with SDF-1α efficiently showed additive effects on the promotion of cell migration from the neurosphere. SJP, fucoidan, or heparin interaction with SDF-1α treatment could increase Nestin expression. SDF-1α modulated by SJP, fucoidan, or heparin activated the CXCR4 receptor and directed cellular migration via the activation of the PI3K/Akt/FOXO3a signaling pathway. Moreover, interaction of SJP, fucoidan, or heparin with SDF-1α effectively promoted NSC migration and induced SDF-1α and CXCR4 expressions. Results suggested that SJP, fucoidan, and heparin might be good candidates for alleviating injury-initiated signals to which NSCs respond.

Purification and characterization of a novel fibrinolytic enzyme from Whitmania pigra Whitman.

A fibrinolytic enzyme was purified from the dry body of Whitmania pigra Whitman. The fibrinolytic enzyme was purified to homogeneity with a yield of 0.003% and a purification of 630.7 fold. The molecular weight of the enzyme was estimated to be 26.7 kDa by reduced sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The enzyme was tested by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS) and it showed that the enzyme was a novel fibrinolytic enzyme. The optimal pH and temperature of the enzyme were 8.5 and 55°C, respectively. Enzyme activity was enhanced by Na+, Mg2+, and K+. On the contrary, the proteolytic activity was significantly inhibited by Mn2+, Fe2+, Fe3+, ethylenediaminetetraacetic acid (EDTA), and ethylenebis(oxyethylenenitrilo)tetraacetic acid (EGTA). Fibrinolytic and fibrinogenolytic assays showed that the enzyme preferentially hydrolyzed fibrinogen Aα-chains, followed by Bß- and γ-chains. The α-, ß-, and γ-γ-chains of fibrin were also degraded by the enzyme.

Effect of earthworm active protein on fibroblast proliferation and its mechanism.

CONTEXT: Earthworms have been used as a traditional medicine in China from thousands of years. In recent years, research has demonstrated that earthworm extracts might promote wound healing; however, its mechanism is still unknown. OBJECTIVE: The study investigates the mechanism and effects of earthworm active protein (EAP), on mouse embryonic fibroblast (NIH/3T3) proliferation. MATERIALS AND METHODS: The effects of earthworm active protein (EAP) in different concentrations (0, 25, 50, 100, 150, and 200 µg/mL) on NIH3T3 cell were detected by the MTT and Brdu incorporation assay (50, 100, and 150 µg/mL). The effects of EAP (37.5, 75, and 150 µg/mL) on the cell cycle were detected by flow cytometry. The cell signaling pathways of EAP-promoting NIH3T3 cell proliferation were studied by the MTT and Western blot by using different signaling pathway inhibitors. RESULTS: The results showed that EAP (50, 100, and 150 µg/mL) could promote NIH3T3 fibroblasts proliferation (36.4 ± 4.4%, 59.1 ± 4.9%, and 71.5 ± 5.7%). The mechanism of EAP promoting NIH3T3 cell proliferation should be as follows: EAP elevated cyclin D1 expression by activating MEK/ERK signaling pathway, and then promoted cell cycle from G1 to S phase, finally caused the proliferation of NIH3T3 cell. PI3K signaling pathway may be the upstream of MEK/ERK signaling pathway. DISCUSSION AND CONCLUSION: The study demonstrates that EAP is effective in promoting effects on proliferation and migration activity of NIH3T3 cell, and the proliferation activity of EAP on NIH3T3 cell may be achieved through the PI3K→Rac→PAK→MEK signaling pathway.

Sulfated Polysaccharide Isolated from the Sea Cucumber Stichopus japonicus Against PC12 Hypoxia/Reoxygenation Injury by Inhibition of the MAPK Signaling Pathway.

In this report, the sulfated polysaccharide (SJP) isolated from the sea cucumber Stichopus japonicus can protect PC12 from Na2S2O4-induced hypoxia/reoxygenation (H/R) injury. SJP effectively improves cell viability and reduces extracellular LDH release in PC12 cells after H/R. Moreover, SJP significantly increases SOD activity but decreases MDA levels. Our experiments showed that SJP could significantly reduce cell apoptosis caused by H/R. Our current results demonstrate that SJP suppressed the activation of MAPKs, resulting in a significant decrease in Bax/Bcl-2 ratio, cleaved caspase-3/caspase-3, p53 phosphorylation, and cytochrome c release in a concentration-dependent manner. MAPK is closely related to H/R injury. SJP inhibited JNK1/2 and p38 MAPK activation but did not affect the increased ERK1/2 expression. These results suggested that JNK1/2 and p38 MAPK pathways could be involved in SJP-mediated attenuation of PC12 H/R injury. SJP prevented PC12 H/R injury in a dose-dependent manner, indicating that SJP may be developed as a candidate drug to prevent or treat cerebral ischemia-reperfusion injury.

An extract from medical leech improve the function of endothelial cells in vitro and attenuates atherosclerosis in ApoE null mice by reducing macrophages in the lesions.

AIM: Medicinal leech has been widely used as a traditional Chinese medicine in cardiovascular diseases. However, its pharmaceutical effect is not fully revealed. The goal of this study was to determine whether a leech extract has the effect of anti-atherosclerosis in ApoE −/− mice and the mechanism of this effect. METHODS AND RESULTS: In vivo experiments: ApoE −/− mice fed on high-cholesterol diet were separated into 5 groups. Control group was administrated with normal water; leech extract of low dose treatment group was given a leech extract of 0.02 g/kg/d; leech extract of medium dose treatment group was given a leech extract of 0.1 g/kg/d; leech extract of high dose treatment group was given a leech extract of 0.5 g/kg/d; simvastatin group was given simvastatin of 10 mg/kg/d. Leech extract significantly reduced atherosclerotic lesions in aortic root compared with control group. And the number of macrophage in or around the atherosclerosis plaque is significantly reduced in the leech extract groups compared with control group. In vitro experiments: human endothelial cell line, EA.hy926, was induced with TNF-α to perform endothelial dysfunction. Control group: EA.hy926 cells with no special treatment; TNF-α group: EA.hy926 cells were induced by 10 ng/ml TNF-α for 6 h; leech extract only group: EA.hy926 cells were treated with 200 mg/ml leech extract only; leech extract and TNF-α group: 200 mg/ml leech extract was applied before TNF-α induction. Protein and mRNA level were detected in each group, leech extract can decrease the expression of intercellular adhesion factor (ICAM-1) and monocyte chemotactic protein (MCP-1) compared with TNF-α group. Furthermore, it showed less adhesion and migration of THP-1 cells to EA.hy926 cells in the adhesion assay and transwell assay. The NF-κB translation to nucleus was blocked by leech extract in the NF-κB translocation assay. CONCLUSIONS: Leech extract could obviously attenuate the area of atherosclerosis lesion in ApoE −/− mice. And this effect is dose dependent. The effect is mainly a result of reduced invasion of monocyte in artery walls by blocking NF-κB translocation.

A novel protein from Eupolyphaga sinensis inhibits adhesion, migration, and invasion of human lung cancer A549 cells.

Eupolyphaga sinensis Walker is an important insect used in Chinese traditional medicine. In this study, we purified a 72-kDa anticancer protein, designated as EPS72, from this species using ammonium sulfate precipitation, ultrafiltration, CM Sepharose Fast Flow cation exchange, Q Sepharose High Performance (HP) anion exchange, Butyl Sepharose HP hydrophobic chromatography, and Superdex 75 gel filtration chromatographic techniques. EPS72 exhibited a potent anticancer activity against the human lung cancer A549 cell line (IC50, 18.76 µg/mL). Further study showed that EPS72 could induce A549 cell detachment and apoptosis, inhibit cell adhesion to fibronectin and collagen IV, and restrain cell migration and invasion. Moreover, EPS72 significantly decreased the expression of ß1-integrin. This study suggests that EPS72 could potentially be developed as a novel anticancer therapeutic agent due to its possible antimetastatic activity.