Fig. 4

Schematic overview of the principal mechanisms and targeted signalling pathways mediated by DBCLS from the Schisandra genus in cancer treatment emphasizing their role in arresting the cell cycle and promoting apoptosis through the mitochondrial pathway and caspase activation. It highlights the induction of cell cycle arrest, particularly in the G1/S and G2/M checkpoints, which leads to a marked decrease in cancer cell proliferation; correspondingly, a significant reduction in cyclin D1 expression is noted, a key regulator of cell cycle progression. Furthermore, DBCLS are shown to enhance apoptotic pathways through mitochondrial perturbations, caspase activation, and cleavage of poly (ADP-ribose) polymerase (PARP), contributing to programmed cell death. They also elevate reactive oxygen species (ROS) within cells, contributing to oxidative stress and potential cellular damage. Simultaneously, the diagram indicates a suppression of the PI3K/Akt/mTOR signaling pathway by DBCLS, which correlates with an increase in autophagic activity, a cellular degradation process that can lead to cell death under certain conditions. Additionally, the ligands inhibit cellular mechanisms responsible for invasion, migration, and metastasis, likely through the modulation of molecules and pathways such as MMP-2, E-cadherin, HIF-1α, FAK, VEGF, and the MAPK pathway. The upregulation of tumor necrosis factor-alpha (TNF-α) further suggests that DBCLS might induce apoptotic signaling pathways. Symbols: ↑ increase, ↓ decrease. Akt Protein kinase B, AMPK AMP-activated protein kinase, Cyt C Cytochrome c, E-cadherin Epithelial cadherin, ERK Extracellular signal-regulated kinase, FAK Focal adhesion kinase, HIF-1α Hypoxia-inducible factor 1-alpha, JNK c-Jun N-terminal kinase, MAPK Mitogen-activated protein kinase, MMP-2 Matrix metalloproteinase-2, mTOR Mammalian target of rapamycin, PARP Poly (ADP-ribose) polymerase, PI3K Phosphoinositide 3-kinase, ROS Reactive oxygen species, STAT-1 Signal transducer and activator of transcription 1, TNF-α Tumor necrosis factor alpha, VEGF Vascular endothelial growth factor