# \(\beta\)-Glucans from Yeast--Immunomodulators from Novel Waste Resources
## 7 Anticancer Properties  
\(\beta\)-glucans do not directly affect cancerous cells and tumours; their anti-cancer effects are elicited through stimulation of the immune response [86]. \(\beta\)-glucans achieve their anti-tumour outcomes by forming a complement complex. After systemic uptake, they are bound by endogenous plasma anti-\(\beta\) glucan antibodies (A.B.A.). This complex activates complement with the complement protein iC3b binding to the A.B.A. [87; 88]. This secondary complex binds to immune cells and triggers different immune responses, includingCR3 phagocytosis, which accelerates the killing of antibody-targeted tumour cells [87,88]. Most medicinal \(\beta\)-glucans contain a (1-3) backbone with (1-6) links [89]. Complexity in structure increases anti-cancer properties [90]. Autophagy is a physiological cellular process that degrades and eliminates misfolded proteins and damaged organelles. It is an intracellular degradative process caused by organelle damage, aberrant proteins, and nutritional shortage. Autophagy regulation is involved in both tumour suppression and tumour promotion. Autophagy also modulates the features of cancer stem cells, contributing to their stemness, recurrence, and resistance to anti-cancer treatments [91]. Proteins, damaged mitochondria, and other organelles swallowed by autophagosomes can be destroyed and recycled in autolysosomes by lysosomal hydrolases [92,93,94]. A study by [PERSON] et al. (2020), discovered an anti-tumour mechanism of water-soluble yeast \(\beta\)-glucan. This study demonstrated that glucans are a natural autophagy inhibitor with high potential in liver cancer treatment for the first time. The polysaccharide inhibited autophagic breakdown by rising lysosomal pH and decreasing the activity of lysosomal cathepsins, resulting in the buildup of damaged mitochondria and the formation of ROS. Additionally, the sugar inhibits hepatocellular carcinoma cell (HCC) metabolism in the glycolysis and tricarboxylic acid (TCA) cycles and induces cell death without nutrients. Further, yeast \(\beta\)-glucan effectively reduced tumour development in a xenograft mouse model and a primary HCC model produced by DEN/CC14 (diethylInitrosamine/carbon tetrachloride) without any damage. The data also indicate that \(\beta\)-glucan is a new autophagy inhibitor with solid anti-tumour activity and potential therapeutic use in the clinical treatment of HCC. In immunodeficient BALB/c nude mice, yeast \(\beta\)-glucan exerted significant anti-tumour activity. The mice lack a thymus and are unable to produce T-cells. This data suggests yeast \(\beta\)-glucan exerted direct anti-tumour effects that were not dependent on the immune system [2]. To ultimately establish the yeast \(\beta\)-glucan putative mechanism of autophagy suppression, autolysosome production and lysosomal activity were investigated. The lysosome's low luminal pH (4-5) is required for lysosomal enzyme activation and cargo breakdown. Increased lysosomal pH has been shown to hinder lysosomal autophagosome fusion. The data in this study suggest that yeast \(\beta\)-glucan limits autophagic flux by rising lysosomal pH and reducing cathepsin activity without impacting autophagosome-lysosomal fusion. Autophagy enhances tumour cell survival under stressful conditions such as hypoxia, food deprivation, and treatment resistance. The results of this study demonstrate yeast \(\beta\)-glucan sensitised apoptosis in nutritional deficient HCCs [2]. Studies are ongoing to find a cure for myelosuppression and boost the immune systems of individuals suffering from chemotherapy-induced myelosuppression. A study by [PERSON] et al. (2019) investigated the level of damage to myeloid and lymphoid cell growth induced by chemotherapy medications. The effect of yeast \(\beta\)-glucan on alleviating immunoprecipitation was studied. I.P. administered gemcitabine at 30 mg/kg was used to reduce red blood cells, white blood cells, and platelets. The treatment also inhibited lymphocyte activity and damaged bone marrow tissue.