In this blog, we will discuss further details about fucoidan’s anti-cancer effect on estrogen receptor (ER) – mediated cancer such as breast cancer, endometrial cancer, and ovarian cancer related to the female hormone. Based on the research “A Fucus versiculosus extract inhibits estrogen receptor activation and induces cell death in female cancer cell lines” by Jianqing Zhang et.al.

Brown seaweed such as Fucus vesiculosus (F. Fucoidan) is widely consumed due to its potential anti-cancer activities and various bioactivities. We have previously detailed anti-estrogen studies in human and animal studies.

In another significant case study, F. Fucoidan administered to pre-menopausal women with endometriosis led to a reduction in circulating estradiol (E2) levels. It also increased the length of the menstrual cycle and diminished symptoms of hypermenorrhea and dysmenorrhea. The researchers acknowledged that this is because of fucoidan’s anti-estrogen effect. We reported that fucoidan’s anti-estrogenic activity is due to the inhibitory activation of enzymes that make estrogen called aromatase or estrogen binding inhibition to estrogen receptor (ER).

They investigated fucoidan’s anti-cancer effect on estrogen receptor (ER) – mediated cancer such as breast cancer, endometrial cancer, and ovarian cancer related to the female hormone.

Their investigation is as follows:

First, they investigated how fucoidan works on activation of ER. Atlantic F. First, Fucoidan was grounded into a fine powder. The foreign substances were removed, and the powder was prepared for F. Fucoidan extraction. Next, E2 was added to the human mammary adenocarcinoma cell line T47D-KBluc, and a test was conducted to fluoresce color when ER was activated. When E2 was added to T47D-KBluc, fluoresce color was started, which meant ER was activated. In the FVE-added group, we observed that the higher the concentration, the lower the fluorescence color, and the lower the ER activation. (Fig. 1)

Next, the effect of cancer was observed by adding F. Fucoidan to a breast cancer cell, endometrial cancer cell, and ovarian cancer cells. The result was that the higher the concentration of F. Fucoidan in any cells, the lesser the survival of cancer cells. (Fig. 2)

Additionally, we further examined the mechanism of action of how F. Fucoidan reduces the survival of cancer cells. To explore apoptosis’s contribution in reducing cell viability by F. Fucoidan, they measured caspase activity in breast cancer cells MDA-MB-231. As a result, caspase activity was increased in F. Fucoidan-treated breast cancer cells MDA-MB-231. (Fig. 3)

As for the reference proved by the research, autophagy deficiencies also activate the DNA damage response in vitro and in vivo breast tumors, promote gene amplification, and synergize with defective apoptosis to accelerate breast tumor formation. Therefore, the loss of autophagy’s role in promoting survival may contribute to breast cancer progression by promoting genomic damage and instability.

Reference: https://www.tandfonline.com/doi/abs/10.4161/auto.4867

Hence, we have demonstrated F. Fucoidan-induced autophagy along with observation of F. Fucoidan induced autophagy in MDA-MB-231 cells. According to the study, we found that F. Fucoidan contains fucoidan involved inhibition of ER activation, which leads to the self-destruction of cancer cells to stimulate apoptosis and autophagy action on female-specific cancer cells.

Reference: https://bmccomplementmedtherapies.biomedcentral.com/articles/10.1186/s12906-016-1129-6