Lonicera japonica Thunb. is a traditional medicinal plant rich in bioactive flavonoids, but the transcriptional regulation of flavonoid biosynthesis remains unclear. In this study, we identified LjMYB106, an R2R3-MYB transcription factor associated with flavonoid accumulation, from floral developmental transcriptomes. Sequence and phylogenetic analyses showed that LjMYB106 contains conserved R2 and R3 MYB domains and is closely related to homologous MYB proteins. Heterologous overexpression of LjMYB106 in Arabidopsis thaliana and Nicotiana benthamiana increased total flavonoid and p-coumaric acid contents. Integrated transcriptomic and widely targeted metabolomic analyses in A. thaliana showed that LjMYB106 overexpression was associated with changes in phenylpropanoid and flavonoid biosynthetic pathways. qRT-PCR validation further showed that PAL, C4H, 4CL, CHS, DFR, and ANS homologs were up-regulated, whereas CHI, F3H, and FLS homologs were down-regulated in LjMYB106-overexpressing plants. Subcellular localization and yeast transactivation assays indicated that LjMYB106 is a nuclear protein with transcriptional activation activity. These results suggest that LjMYB106 is a candidate regulator of phenylpropanoid and flavonoid metabolism and provide a basis for further studies of MYB-mediated flavonoid regulation in L. japonica.
Jiangxin Yang, Jingjie Zhang, Xing-Yu Nie et al.· Frontiers in Plant Science· 0 citations
Background: Colorectal cancer (CRC) is one of the most common and lethal malignancies worldwide, with rising incidence and limited therapeutic options. Traditional Chinese medicine (TCM) formulations, known for their multi-component and multi-target synergistic actions, offer a promising alternative or adjunctive strategy. Ginger jujube tea (GJT), a classic TCM decoction, has been historically used for gastrointestinal regulation, yet its anti-CRC efficacy and pharmacological mechanisms remain unexplored. Methods: An integrated network pharmacology approach was employed to predict the active constituents of GJT and their potential CRC-related targets, followed by molecular docking to validate key compound-target interactions. The predicted pathways were further investigated through in vitro experiments using CRC cell lines (proliferation assays, reactive oxygen species (ROS) detection, apoptosis evaluation) and in vivo studies in a CRC xenograft mouse model, where tumor growth inhibition, safety profiles, and mechanistic markers (MAPK1, ESR1, HIF1A, PI3K-AKT pathway) were assessed. Results: Network pharmacology and molecular docking identified quercetin, naringenin, and other bioactive compounds as major active components, with core targets including AKT1, MAPK1, and ESR1 , predominantly enriched in the PI3K-AKT signaling pathway. In vitro , GJT dose-dependently suppressed CRC cell proliferation, significantly elevated intracellular ROS levels, and induced apoptosis. In vivo , GJT at 10 g/kg achieved a robust tumor growth inhibition rate of 64.69 ± 6.95% without observable toxicity, as confirmed by biochemical and histopathological analyses. Mechanistically, GJT downregulated MAPK1, ESR1, and HIF1A expression and inhibited PI3K-AKT pathway activation, corroborating the network-based predictions. Conclusion: GJT exerts potent anti-CRC effects through a multi-component, multi-target, and multi-pathway mechanism, consistent with the holistic philosophy of TCM. The favorable efficacy and safety profile support its potential as a complementary therapeutic candidate for CRC, warranting further clinical investigation.
Xing-Yu Nie, Li-Yi Fang, Yu-Qing Cui et al.· Cancer Advances· 0 citations