In the following blog post, I will be focusing on the effects of fucoidan specifically on Oral Squamous Cell Carcinoma (OSCC). The study, “Antitumor Effects of Fucoidan Via Apoptotic and Autophagic Induction on HSC-3 Oral Squamous CellCarcinoma” by Pathanin Chantree et al., revealed that fucoidan can suppress the growth and proliferation of HSC-3 oral squamous cell carcinoma through inducing apoptosis, autophagy, and cell cycle arrest.
Among the various types of cancers that can lead to mortality on a global scale, oral squamous cell carcinoma (OSCC) stands out, and even with numerous advancements in treatment over the years, the outlook for OSCC patients continues to range from moderate to poor. The survival rates have seen a moderate increase over the course of the last 30 years. Standard treatments for oral cancer include surgery, radiation therapy, and chemotherapy can also be used as a treatment, but its side effects can lead to controversial results. In a concerning finding, approximately 50% of patients diagnosed with locally advanced OSCC face the unfortunate outcome of treatment resistance, leading to either recurrence or the formation of distant metastases. Hence, the demand for the formulation of a chemotherapeutic agent that is both highly effective and minimizes side effects, particularly if derived from natural sources, persists.
Fucoidan, a sulfated polysaccharide found naturally, has been the subject of multiple studies that have consistently shown its remarkable effects, including antioxidant, anticoagulant, anti-inflammatory, and anticancer effects. Additionally, one of the advantages of fucoidan is its complete absence of side effects.
Autophagy serves a dual role, acting both as a protective mechanism for cell survival and as a pro-apoptotic mechanism for cell death triggered by external stimuli. Autophagy is a complex cellular process in which the cellular contents are enclosed within autophagosomes. These autophagosomes then undergo fusion with lysosomes, leading to the degradation and breakdown of the components. Earlier studies have proposed that chemotherapy treatment triggers autophagy in cancer. The purpose of this study was to examine the antitumor effects of a purified form of fucoidan that was extracted from Fucus fucoidan. The specific focus was on its effects on HSC-3 oral squamous cell carcinoma, as well as the underlying molecular mechanisms involved. The result of this study offers scientific evidence that suggests fucoidan could be used in the treatment of oral cancer in the future.
First, HSC-3 cells were treated with 0, 100, 200, and 400 μg/mL fucoidan, and cell viability was measured using MTT assay. The result was after treatment with fucoidan for 24 h, the cell viability (%) of HSC-3 cells decreased from 10 to 400 μg/ml in a concentration-dependent manner compared to the control group. (See Figure 1A)
The assessment of apoptosis and cell cycle involved the use of flow cytometry-based assays. Chromatin condensation and nuclear fragmentation were measured using Hoechst 33342 staining, and mitochondrial membrane potential (ΔΨm) was measured using the JC-1 kit. The investigation of apoptotic, anti-apoptotic, and autophagic markers involved performing Western blot analysis.
The viable cell number of treated HSC-3 cells was reduced. Also, treated cells were arrested in her G0/G1 phase. Annexin V/PI staining revealed that fucoidan could induce apoptosis in HSC-3 cells. Moreover, the data obtained from this study revealed a significant rise in the percentage of treated cells that were observed to be in the early and late stages of apoptosis after being treated with 100, 200, and 400 μg/ml fucoidan (as indicated in Figure 2E). The study confirmed that fucoidan can induce apoptosis in HSC-3 cells. Western blot analysis suggested upregulation of apoptotic markers, including cleaved caspase-3, cleaved PARP, Bax, and autophagy markers such as LC3-II and Beclin-1, whereas the anti-apoptotic marker Bcl- Downregulation of 2 was suggested. Fucoidan can interfere with ΔΨm and induce chromatin condensation with nuclear fragmentation.
Following the treatment of fucoidan, granules and vacuoles became evident on the cell surface and cytoplasm of HSC-3 cells. The amounts of these morphological changes were developed in a concentration-dependent manner. Furthermore, to evaluate whether granular and vacuole appearances were involved with autophagy, LC3-II, and Beclin-1, which are the protein markers for autophagy, were examined. It was observed in the study that the levels of LC3-II and Beclin-1 showed a significant concentration-dependent increase following the treatment. (See Figure. 3 E) Fucoidan could induce autophagy in HSC-3 cells.
In conclusion, these results showed Fucoidan has potential anticancer properties against HSC-3 cells by induction of apoptosis, cell cycle arrest, and autophagy. The study also indicated that Fucoidan has potential anticancer properties against HSC-3 cells.
Source: Asian Pac J Cancer Prev. 2020 Aug; 21(8): 2469–2477. doi: 10.31557/APJCP.2020.21.8.2469
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