Chemical Compounds, Bioactivities, and Potential Applications of the Mushroom Species of Genus Suillus (Agaricomycetes): A Review.

The genus Suillus, also known as "Song mo," falls under the order Boletales and consists of various higher fungi. It establishes mycorrhizae primarily with pine trees and has a good taste and medicinal values. Herein, we reviewed the chemical compounds present in the genus Suillus, including polysaccharides, steroids, phenols, polyprenyl phenol derivatives, fatty acids, organic acids, and amino acids, and their reported bioactivities and potential applications. This review aims to promote the utilization of the resources belonging to the genus Suillus and serves as a theoretical basis for their future studies and clinical applications.

Galangin inhibits programmed cell death-ligand 1 expression by suppressing STAT3 and MYC and enhances T cell tumor-killing activity.

BACKGROUND: The flavonoid galangin (3,5,7-trihydroxyflavone) is derived from the root of Alpinia officinarum Hance, an edible and medicinal herb. Galangin has many biological activities, such as anti-inflammatory, anti-microbial, anti-viral, anti-obesogenic, and anti-oxidant effects. However, the anti-tumor mechanism of galangin remains unclear. PURPOSE: To elucidate the anti-tumor mechanisms of galangin in vitro and in vivo. METHODS: MTT, western blotting, immunoprecipitation, RT-PCR, and immunofluorescence assays were used to assess the mechanism of galangin inhibiting PD-L1 expression. The effect of galangin on T cell activity was analyzed in Hep3B/T cell co-cultures. Colony formation, EdU, migration, and invasion assays were performed to explore the effect of galangin on cancer progression and metastasis. Anti-tumor effects of galangin were investigated in a xenograft model. RESULTS: Galangin inhibited PD-L1 expression dose-dependently, which plays a major role in tumor progression. Moreover, galangin blocked STAT3 activation through the JAK1/JAK2/Src signaling pathway and Myc activation through the Ras/RAF/MEK/ERK signaling pathway. Galangin reduced PD-L1 expression by suppressing STAT3 and Myc cooperatively. Galangin increased the killing effect of T cells on tumor cells in Hep3B/T cell co-cultures. Moreover, galangin inhibited tumor cell proliferation, migration, and invasion through PD-L1. In vivo experiments showed that galangin suppressed tumor growth. CONCLUSION: Galangin enhances T-cell activity and inhibits tumor cell proliferation, migration, and invasion through PD-L1. The current study emphasizes the anti-tumor properties of galangin, offering new insights into the development of tumor therapeutics targeting PD-L1.