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  • Writer's pictureInfinitum Health Team

Anti-tumor and anti-angiogenic effects of Fucoidan on Prostate Cancer

An amazing new study on the effects of Fucoidan on Prostate Cancer further validate its capabilities for anti-tumor and anti-angiogenic effects (1)! More research is still needed, but this study seems to articulate a specific pathway, JAK-STAT3, that is significantly disrupted during Fucoidan treatment. For the non-technical audience, the JAK-STAT3 pathway is a target of angiogenesis-mediated cancer therapy and is crucial in understanding how Fucoidan seems to disrupt this process. Angiogenisis is the physiological process through which new blood vessels form from pre-existing vessels, effectively, how cancer can grow from itself.

Whats even more exciting for us here at Infinitum Health, is this study used DU-145 Prostate cancer cell lines, the exact same National Institutes of Health (NIH) approved cell line that we at Infinitum Health used in our proof of concept in vitro study using Infinimin® (2)

Prostate cancer is the most common cancer in men in the United States. Fucoidan is a bioactive polysaccharide extracted mainly from brown seaweeds. The purpose of this study was to investigate anti-tumor and anti-angiogenic effects of fucoidan in both cell-based assays and mouse xenograft model (taking cells from one and transferring to another, in this case, cancerous cells into a mouse model), as well as to clarify possible role of JAK-STAT3 pathway (3, 4).

Infinitum Health Disclaimer: Reader beware, about to get technical. We try not to dilute the science out of respect to the investigators as well as our customers. We hope that providing the detail, we will empower our customers to become more informed on these processes so that they can make better decisions around their health.

DU-145 human prostate cancer cells were treated with 100–1000 μg/mL of fucoidan. Cell viability, proliferation, migration and tube formation were studied using MTT, EdU, Transwell and Matrigel assays, respectively (See Figure 2 below).

Athymic nude mice were subcutaneously injected with DU-145 cells to induce the xenograft model, and treated by oral gavage with 20 mg/kg of fucoidan for 28 days. Athymic means "without a thymus" - these are immunodeficient mice originated from NIH and approved for research purposes only. Being immunodeficient can speed up the process of understanding cancers in these cell systems. A great company providing these research models is Charles River's Labs.

Tumor volume and weight were recorded. Vascular density in tumor tissue was determined by hemoglobin assay and endothelium biomarker analysis (See Figure 3 below).

Protein expression and phosphorylation of JAK and STAT3 were determined by Western blot. Activation of gene promoters was investigated by chromatin Immunoprecipitation.

Don't know what a hemoglobin assay, endothelium biomarkers, phosphorylation, Western blot or chromatin immunoprecipitation is? Google does. Make sure to read up and understand the science. Knowledge is power.

Fucoidan dose-dependently inhibited cell viability and proliferation of DU-145 cells as well as inhibited cell migration. In the mouse study, 28-day treatment of fucoidan significantly reduced the tumor growth and inhibited angiogenesis, with decreased hemoglobin content and reduced mRNA expression of CD31 and CD105 in tumor tissue. Furthermore, phosphorylated JAK and STAT3 in tumor tissue were both reduced after fucoidan treatment, and promoter activation of STAT3-regulated genes, such as VEGF, Bcl-xL and Cyclin D1, was also significantly reduced after treatment.

This is a remarkable study, which excitedly, further validates what we here at Infinitum Health have begun in our research program proving our products and their efficacy!!

As always, more work moving in the clinical (human) model is needed, but these are great foundational studies to provide a more confident step forward in the research.

We congratulate the investigators on an excellent study and addition to the knowledge in this field.


2. Gao L, Alumkal J. Epigenetic regulation of androgen receptor signaling in prostate cancer. Epigenetics. 2011;5(2):100.

3. Rodriguez C, Patel AV, Calle EE, Jacobs EJ, Chao A, Thun MJ. Body mass index, height, and prostate cancer mortality in two large cohorts of adult men in the United States. Cancer Epidemiol Biomark Prev. 2001;10(4):345

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