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A noteworthy group of culinary and medicinal plants is Polygonatum species. They are known for their abundant flavonoid compound-rich rhizomes, which have antioxidative and anticancer activities. Using Polygonatum sibiricum Red (SXHZ) and Polygonatum kingianum var. grandifolium (HBES), we conducted transcriptome and metabolomic investigations to look into the molecular processes that control the manufacture of these flavonoids in Polygonatum plants. Seven distinct flavonoid metabolites were identified by the analytical data, with phloretin exhibiting a notable differential expression in the biosynthetic pathway. 30 genes with differential expression were found in both plants after further investigation, five of which are members of the transcription factor family associated with MBW. Thus, we suggest that Phloretin and the genes belonging to the MYB-related transcription factor family play a crucial role in controlling the flavonoid biosynthesis pathway in Polygonatum . This work lays the groundwork for a deeper comprehension of the biosynthesis and metabolic processes of flavonoids in Polygonatum , serving as an invaluable resource for the development of the polygonatum -related pharmaceutical industries as well as for the future breeding of Polygonatum plants with higher flavonoid content.

Broadly targeted metabolomics techniques were used to identify phenolic acid compounds in Polygonatum kingianum var. grandifolium (PKVG) rhizomes and retrieve anti-cancer/tumor active substance bases from them. We identified potential drug targets by constructing Venn diagrams of compound and disease targets. Further, KEGG pathway analysis was performed to reveal the relevant pathways for anti-cancer/tumor activity of PKVG. Finally, we performed molecular docking to determine whether the identified proteins were targets of phenolic acid compounds from PKVG rhizome parts. The study’s results revealed 71 phenolic acid compounds in PKVG rhizomes. Among them, three active ingredients and 42 corresponding targets were closely related to the anticancer/tumor activities of PKVG rhizome site phenolic acids. We identified two essential compounds and eight important targets by constructing the compound-target pathway network. 2 essential compounds were androsin and chlorogenic acid; 8 key targets were MAPK1, EGFR, PRKCA, MAPK10, GSK3B, CASP3, CASP8, and MMP9. The analysis of the KEGG pathway identified 42 anti-cancer/tumor-related pathways. In order of degree, we performed molecular docking on two essential compounds and the top 4 targets, MAPK1, EGFR, PRKCA, and MAPK10, to further validate the network pharmacology screening results. The molecular docking results were consistent with the network pharmacology results. Therefore, we suggest that the phenolic acids in PKVG rhizomes may exert anti-cancer/tumor activity through a multi-component, multi-target, and multi-channel mechanism of action.

Sweet potatoes are rich in amino acids, organic acids, and lipids, offering exceptional nutritional value. To accurately select varieties with higher nutritional value, we employed liquid chromatography–tandem mass spectrometry (LC-MS/MS) to analyze the metabolic profiles of three types of sweet potatoes (white sweet potato flesh, BS; orange sweet potato flesh, CS; and purple sweet potato flesh, ZS). When comparing CS vs. BS, ZS vs. BS, and ZS vs. CS, we found differences in 527 types of amino acids and their derivatives, 556 kinds of organic acids, and 39 types of lipids. After excluding the derivatives, we found 6 amino acids essential for humans across the three sweet potatoes, with 1 amino acid, 11 organic acids, and 2 lipids being detected for the first time. CS had a higher content of essential amino acids, while ZS had a lower content. Succinic acid served as a characteristic metabolite for ZS, helping to distinguish it from the other two varieties. These findings provide a theoretical basis for assessing the nutritional value of sweet potatoes and setting breeding targets while facilitating the selection of optimal varieties for food processing, medicine, and plant breeding.

Liver cancer remains a smajor cause of mortality worldwide, underscoring the urgent need for novel natural therapeutics. Polygonatum kingianum var. grandifolium (PK) and Polygonatum sibiricum Redouté (PS) are rice in terpenoids, yet their anti-liver cancer mechanisms remain poorly understood. This study used metabolism, network analysis, molecular docking, and molecular dynamics simulations to investigate their therapeutic potential. Metabolomic analysis identified nine differential terpenoid metabolites, with Maslinic acid and Alphitolic acid being species-specific. Network analysis revealed 23 liver cancer-related targets, including five key proteins: HMGCR, PTGS2, ESR1, PPARG, and PGR. Functional enrichment analysis identified 126 GO terms and 11 KEGG pathways ( P  < 0.05). Molecular docking suggested strong binding affinities between core compounds and targets, while molecular dynamics simulations confirmed the stability of maslinic acid and alphitolic acid with their respective targets. This study enhances the pharmacological understanding of Polygonatum species and offers promising insights for the development of novel liver cancer treatments.

Activating RAS mutations are found in a subset of fusion-negative rhabdomyosarcoma (RMS), and therapeutic strategies to directly target RAS in these tumors have been investigated, without clinical success to date. A potential strategy to inhibit oncogenic RAS activity is the disruption of RAS prenylation, an obligate step for RAS membrane localization and effector pathway signaling, through inhibition of farnesyltransferase (FTase). Of the major RAS family members, HRAS is uniquely dependent on FTase for prenylation, whereas NRAS and KRAS can utilize geranylgeranyl transferase as a bypass prenylation mechanism. Tumors driven by oncogenic HRAS may therefore be uniquely sensitive to FTase inhibition. To investigate the mutation-specific effects of FTase inhibition in RMS we utilized tipifarnib, a potent and selective FTase inhibitor, in in vitro and in vivo models of RMS genomically characterized for RAS mutation status. Tipifarnib reduced HRAS processing, and plasma membrane localization leading to decreased GTP-bound HRAS and decreased signaling through RAS effector pathways. In HRAS-mutant cell lines, tipifarnib reduced two-dimensional and three-dimensional cell growth, and in vivo treatment with tipifarnib resulted in tumor growth inhibition exclusively in HRAS-mutant RMS xenografts. Our data suggest that small molecule inhibition of FTase is active in HRAS-driven RMS and may represent an effective therapeutic strategy for a genomically-defined subset of patients with RMS.

Selenium nanoparticles (SeNPs) can be absorbed by plants, thereby affecting plant physiological activity, regulating gene expression, and altering metabolite content. However, the molecular mechanisms by which exogenous selenium affects Polygonatum kingianum coll.et Hemsl plant secondary metabolites remain unclear. In this study, we exposed P. kingianum plants to SeNPs at 0, 10, 25, and 50 mg/L concentrations. Joint physiological, metabolomic, and transcriptomic analyses were performed to reveal the response mechanisms of major secondary metabolites of P. kingianum to SeNPs. Our data shows that under the treatment of 25 mg/L, the photosynthetic electron transfer rate of plants significantly increases and the carbon-nitrogen ratio significantly decreases. In parallel, the main active components, polysaccharides and saponins, showed a significant increase in content, while flavonoid content decreased. SeNPs affect polysaccharide accumulation mainly through up-regulation of SPS, UGPase, AGPase, UTP, and SUS genes in starch and sucrose metabolic pathways. The accumulation of saponins was affected by upregulating genes in the sesquiterpenoid and triterpenoid biosynthesis pathways, including PAD, ADH, PK, and GS. The accumulation of flavonoids was mainly regulated by metabolic pathways such as flavonoid biosynthesis, isoflavonoid biosynthesis, and the biosynthesis of phenylpropanoids. In summary, this study reveals the key metabolic pathways affected by SeNPs in the main secondary metabolic products of P. kingianum .

Constitutive activation of Akt has been found in many types of human cancer, and is believed to promote proliferation and increased cell survival thereby contributing to cancer progression. In this study, we examined Akt phosphorylation on Ser473 and Thr308 in seven IGF-II-overexpressing rhabdomyosarcomas (RMS) cells. All the RMS cell lines tested had high levels of Akt phosphorylation on Thr308, whereas three cell lines (Rh5, Rh18, and CTR) had a much lower level of Akt phosphorylation on Ser473. To determine whether the difference in Akt phosphorylation on Ser473, but not on Thr308, observed among cell lines is a cell-specific phenomenon or due to other factors, which possibly downregulate Akt phosphorylation, we examined expression of PTEN protein, which acts as a negative regulator of the PI3K/Akt signaling pathway through its ability to dephosphorylate phosphatidylinositol 3,4,5-triphosphate (PIP 3 ). The levels of PTEN expression inversely correlate with Akt phosphorylation on Ser473, but not on Thr308. Consistent with this finding, transfection of wild-type PTEN into RMS and mouse myoblast C2C12 cells resulted in reduced Akt phosphorylation on Ser473, but not on Thr308. Our data suggest that Ser473 may be a key target residue for PTEN to modulate the effects of IGF-II on activating the PI3K/Akt pathway in RMS cells. A better understanding of the pathway in RMS will likely contribute to insights into the biology of the RMS tumorigenesis and hopefully lead to novel therapeutic options.