Introduction: Honeysuckle (Lonicera japonica Thunb.) is a key medicinal plant whose bioactive flavonoids underpin its antiviral, anti-inflammatory, and antioxidant properties. However, the genetic and metabolic mechanisms controlling flavonoid accumulation and the associated flower color variation between different cultivars remain largely unexplored, limiting targeted breeding for enhanced therapeutic quality.Methods: A comparative analysis was conducted using two distinct honeysuckle varieties—'Luyu No.1' (white-yellow flowers) and 'Honghua' (red-pink flowers)—at the optimal harvest stage ('Dabai period'). An integrated transcriptomics (RNA-seq) and widely targeted metabolomics approach was employed to identify differentially expressed genes (DEGs) and differentially accumulated metabolites (DAMs) between the varieties.Results: Transcriptomic profiling revealed 5,901 DEGs, with significant enrichment in the phenylpropanoid and flavonoid biosynthesis pathways. Key structural genes (PAL, CHS, F3H, FLS, DFR, and ANS) were markedly up-regulated in 'Honghua'. Metabolomic analysis identified 399 flavonoids, including 228 DAMs. The 'Honghua' variety exhibited a 2.32-fold higher total flavonoid content, with substantially elevated levels of anthocyanidins (87.58-fold), flavanols (7.66-fold), and chalcones (6.17-fold). Critical medicinal compounds such as quercetin-3-O-rhamnoside and luteolin-7-O-glucoside were significantly enriched in 'Honghua'. Integrated analysis highlighted the co-expression of transcription factors (MYB, bHLH, NAC) with flavonoid pathways. Crucially, the anthocyanin-modifying enzymes F3’M and 3RT were up-regulated by 22.12- and 3.03-fold, respectively, in 'Honghua', while a potential repressor, TCP15 (bHLH), was down-regulated.Discussion: The results demonstrate that the red-pink pigmentation and superior medicinal quality of 'Honghua' are driven by a coordinated gene-metabolite network that fluxes metabolic intermediates towards anthocyanin and other flavonoid end-products. The pronounced up-regulation of F3’M and 3RT is identified as a key biochemical determinant for anthocyanin diversification and color development. This study provides the first comprehensive framework for flavonoid biosynthesis in honeysuckle, establishing a genetic basis for breeding cultivars with high flavonoid content and enhanced pharmacological value.

Sugars are crucial factors that contribute to fruit flavor. To uncover the regulatory mechanism of sugar metabolism in developing fruit, we isolated four genes, encoding key enzymes (sucrose...

Phytosterols (PS) have specific oxidation rules in different lipid media. After oxidation, PS will form oxidation products, which has potential physiological toxicity to the human body. Camellia seed oil (CSO) is a unique emerging edible oil in China. This oil has a fatty acid composition similar to olive oil, in which oleic acid is dominant. In order to solve the thermal oxidation of PS in CSO at high temperature (180 °C), we studied its antioxidant strategy by evaluating different antioxidants. Four antioxidants—BHA, TBHQ, epigallocatechin gallate (EGCG), and α-tocopherol (VE)—along with one synergist, citric acid (CA), were selected and used in this study. The antioxidant effects of different combinations (single antioxidant, single antioxidant + CA, mixed antioxidant, mixed antioxidant + CA) were compared. After 180 min of heating, the PS and phytosterols oxidation products (7α-hydroxy-, 7β-hydroxy-, 5α,6α-epoxy-, 5β,6β-epoxy-, 7-keto-, and trihydroxy-PS) were estimated by GC-MS. Through comparative analysis, the results showed that the combination of mixed antioxidants and CA had the best antioxidant effect, and the inhibition rate of VE + TBHQ +CA was as high as 42%, which had a breakthrough significance for stabilizing the thermal oxidation of PS in camellia seed oil. At the same time, it also provides a valuable reference for ensuring the edible safety of camellia seed oil in Chinese food heating habits.

By combining transcriptome sequencing with single-cell transcriptomic analysis of the tumor microenvironment, we aim to elucidate the molecular mechanisms underlying SerpinB2 (plasminogen activator inhibitor type 2, PAI-2) in regulating glioma cell proliferation. The CGGA and TISCH databases were used to analyze SerpinB2 expression in glioma tissues. The effect of SerpinB2 on the proliferation and migration of glioma cells was determined using CCK-8 and wound healing assays. The signaling pathways potentially regulated by SerpinB2 in glioma cells were analyzed using transcriptome sequencing and single-cell sequencing. Flow cytometry identified the cell cycle of the cells. The expression of cell cycle and Wnt/β-catenin signaling pathway-related mRNA and proteins was determined using q-PCR and Western blotting. Finally, the effect of SerpinB2 on glioma proliferation was verified by constructing a tumor-bearing mouse model. SerpinB2 was highly expressed in malignant glioma tissues and was associated with low patient survival rates. Lv-SerpinB2 enhanced the proliferation and migration of glioma cells. Transcriptome data demonstrated that SerpinB2 regulates the cell cycle. Flow cytometry revealed that SerpinB2 keeps glioma cells in the S phase. The Western blotting results confirmed that the cell cycle-related proteins CCND1, CDK4, and the Wnt/β-catenin signaling pathway proteins β-catenin, Wnt-5a, and C-myc all exhibited increased levels. The tumor-bearing mouse model demonstrated that SerpinB2 promoted the growth of glioma in the Lv-SerpinB2 group. SerpinB2 promotes the proliferation of glioma cells by regulating the cell cycle through the Wnt/β-catenin signaling pathway.

Objectives: Heat shock protein family A (Hsp70) member 9 (HSPA9) is a mitochondrial chaperone protein that belongs to the heat shock protein 70 family. HSPA9 is expressed across various malignancies. However, the intricate relationship and mechanisms between HSPA9 and glioma remain unclear. This study aims to elucidate the molecular mechanisms by which HSPA9 influences glioma progression through transcriptomic and proteomic analysis. Methods: HSPA9 expression in glioma patient tissues was validated by histopathological analysis and Western blotting. Subsequently, stable HSPA9-overexpressing and HSPA9-knockdown U-87 MG and U251 MG cell lines were generated. To investigate the downstream effects, transcriptomic and proteomic sequencing was performed on HSPA9-knockdown U-87 MG cells. Bioinformatics analysis was then applied to identify enriched pathways associated with the differentially expressed genes and proteins. Finally, key metabolites related to these pathways were quantified. Results: Immunohistochemistry and Western blotting revealed a significant elevation of HSPA9 expression in glioma tissues, indicating its potential as a molecular marker for this malignancy. Integrated transcriptomic-proteomic analysis detected 496 downregulated genes and 276 upregulated proteins in HSPA9-knockdown U-87 MG cells. Pathway enrichment analysis indicated that these differentially expressed molecules were primarily enriched in energy metabolism-related pathways. Metabolic assays using commercial kits demonstrated that knockdown of HSPA9 reduced lactate levels in both U-87 MG and U251 MG cells, accompanied by increased glucose and ATP levels. Conversely, in HSPA9-overexpressing U-87 MG and U251 MG cell lines, α-ketoglutarate (α-KG) levels were consistently decreased. Conclusion: The results demonstrated that HSPA9 could drive glioma cells from oxidative phosphorylation toward glycolytic metabolism, thereby accelerating tumor cell proliferation. This study provides novel insights into the influence of HSPA9 on the initiation and progression of glioma through gene and protein expression. Further research needs to be conducted to investigate the potential therapeutic target of HSPA9 in glioma.