Dendrobium officinale polysaccharides

We investigated the carcinogenic effects of four endocrine-disrupting chemicals-bisphenol A (BPA), diethyl phthalate (DEP), dimethyl phthalate (DMP), and dioctyl phthalate (DOP)-in nasopharyngeal carcinoma (NPC) and thyroid carcinoma (THCA) using an integrated toxicogenomic-machine learning-docking-experimental pipeline. Intersection analysis identified 31 NPC-related overlapping genes and 39 THCA-related overlapping genes, with 19 shared core targets across both malignancies. These shared targets were enriched in oncogenic signaling pathways including Mitogen-activated protein kinase （MAPK）, Phosphoinositide 3-Kinase-Protein Kinase B (PI3K-AKT), and Janus kinase/signal transducers and activators of transcription (JAK/STAT). A multi-algorithm machine learning framework constructed 113 predictive models and prioritized six diagnostic genes (CCNA2, CDK2, MET, F2, TYMS, PPARG). High expression of CCNA2 (HR=1.43, p = 0.016), CDK2 (HR=1.66, p = 0.002), MET (HR=1.58, p = 0.002), and PPARG (HR=1.45, p = 0.0072) was associated with worse overall survival, whereas TYMS and F2 were not significant. Molecular docking showed stable ligand-protein binding with energies from -5.2 to -8.1 kcal·mol⁻¹ , with the strongest affinities observed for BPA-CDK2 (-8.1) and BPA-PPARG (-8.1); DEP also showed strong binding to CDK2 (-7.0). In vitro, BPA and DEP (but not DMP/DOP) increased colony formation (p < 0.01), accelerated wound closure, upregulated oncogenic genes (e.g., CDK2/MET/CCNA2; p < 0.05), and elevated p-MEK without changing total MEK in 5-8 F and TPC-1 cells. Collectively, BPA and DEP promote head and neck tumor progression through MEK pathway activation and cell-cycle dysregulation.

Dendrobium officinale polysaccharides (DOP) exhibit anticancer potential against colorectal cancer (CRC), yet their mechanisms remain unclear. This study investigated DOP's effects on HCT‐116 cells. DOP dose‐ and time‐dependently inhibited proliferation and induced apoptosis, evidenced by elevated cleaved caspase‐3/‐9, poly ADP‐ribose polymerase (PARP), Bax, and reduced Bcl‐2. Concurrently, DOP activated autophagy (increased LC3‐II/I, Beclin‐1; decreased p62) via phosphatidylinositol‐3‐kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) suppression. Combining DOP with the autophagy inhibitor chloroquine enhanced apoptosis (higher cleaved PARP, Bax; lower Bcl‐2) and reactivated PI3K/Akt/mTOR signaling. These findings demonstrate DOP inhibits CRC by dual induction of apoptosis and autophagy blockade through PI3K/Akt/mTOR inhibition, with autophagy suppression synergistically augmenting apoptosis. The study highlights DOP's translational potential as a functional food or adjuvant therapy, proposing a novel combinatorial strategy for CRC treatment.