1. In Table 1, why are the mechanisms of action for Agaricus bisporus WAAP-1 and WAAP-2 described identically (upregulation of Caspase-3, BAX, E-cadherin; downregulation of Bcl-2, Vimentin) despite having different molecular weights (10.1 kDa vs. 121 kDa) and structural conformations? This suggests potential oversimplification of distinct compounds’ mechanisms.
2. The paper claims that “fungi could offer unique phenolics and potentially higher bioactivity” compared to plants (Section 2.4.3), yet provides no comparative bioavailability data in human models. What specific evidence supports this assertion beyond in vitro antioxidant assays?
3. In Section 3.10.2, you discuss hTERT modulation citing a study on Ganoderma tsugae in A549 lung adenocarcinoma cells (Reference 125), not colon cancer cells. How is this extrapolation to colon cancer mechanistically justified?