Lung cancer morbidity and mortality rates have been increasing each year. It has a 5-year survival rate of only 18% for non-small cell lung cancer (NSCLC), which accounts for 80-85% of lung cancers. Although there are cases in which chemotherapy and molecular-targeted drugs are effective, the side effects are severe. Additionally, only a few people often have a tolerance for medications.

On a positive note, fucoidan has no side effects and is attracting attention for its anti-cancer benefits. In vitro, cell culture tests have reported that fucoidan has an antitumor effect against head and neck squamous cell carcinoma HNSCC, human breast cancer MCF-7, human colorectal cancer DU145, and hepatocellular carcinoma HCC. However, the tumor suppressive effect of fucoidan on NSCLC has not been clarified yet.

Hence, in this blog, I would like to inform the study “Antitumor effect and molecular mechanism of fucoidan in NSCLC” by Xiaohan Chen et al. They studied the effects of fucoidan on NSCLC using human alveolar basal epithelial adenocarcinoma cells A549 and human lung adenocarcinoma cells H1650, which are NSCLC model cells. Therefore, I would like to share Xiaohan Chen et al. observations.

First, fucoidan was added to A549 and H1650 cells at concentrations of 0, 10, and 16 mg/ml and cultured for 96 hours. (See Figure. 1) Next, they examined the activation state of the signaling pathway involving the mammalian rapamycin target protein mTOR to clarify the molecular mechanism of action by which fucoidan inhibits cancer growth in NSCLC cells. The mTOR signaling pathway is deeply involved in cancer cell proliferation and metastasis, and phosphorylated mTOR, pmTOR, is known to be the active form. Then Western blotting was used to measure the expression levels of phosphorylated proteins. It was found that the expression of pmTOR and pmTOR-related proteins were regulated in fucoidan-added cultures compared to fucoidan-free cultures. (See Figure. 2)

Furthermore, when they checked the fucoidan-treated cells with a flow cytometer capable of examining the viability of individual cells, they found that they had undergone apoptosis. These results suggest that fucoidan suppresses the activation of the mTOR signaling pathway for A549 and H1650, thereby suppressing cellular properties such as promoting cell proliferation and inhibiting apoptosis.

In animal experiments, A549 was implanted in the right armpit of mice, divided into a group receiving 25 mg/kg fucoidan and a group receiving water (control group), and observed for 14 days. As a result, the fucoidan intake group showed significantly smaller tumor formation than the control group. (See Figure. 3) This study proves that fucoidan has an antitumor effect on NSCLC cells both in vitro and in vivo. Hence it is expected to help NSCLC treatment without side effects.

Source: Chen et al. BMC Complementary Medicine and Therapies (2021) 21:25