Bone tissue engineering has been continuously developing since the concept of “tissue engineering” has been proposed. Biomaterials, as the basic material for the fabrication of scaffolds, play a vital role in bone tissue engineering.

Hepatocellular carcinoma (HCC), often arising from liver fibrosis in nonalcoholic fatty liver disease (NAFLD), remains a leading cause of cancer-related death. Targeting the gut–liver axis offers new therapeutic opportunities to prevent this progression. In this study, colon-targeted chitosan/pectin-based nanoparticles loaded with Astragalus polysaccharide (APs-CS/PT-NPs) were developed to modulate gut microbiota and inhibit liver tumorigenesis. The nanoparticles exhibited robust physicochemical stability and pH-responsive release. In vivo, oral administration of APs-CS/PT-NPs attenuated hepatic steatosis, reduced inflammatory cytokines, and suppressed NAFLD-induced HCC development. 16 S rRNA sequencing revealed restoration of microbial diversity and enhanced production of short-chain fatty acids, especially acetate. Mechanistically, transcriptomic profiling and functional analysis identified acetate as a key mediator, acting via G-protein-coupled receptor 43 (GPR43) to inhibit the NF-κB pathway. These results highlight the therapeutic potential of APs-CS/PT-NPs in modulating the gut–liver axis, rebalancing intestinal microbiota, and suppressing pro-inflammatory signaling. This nanoparticle-based strategy offers a promising food-derived preventive intervention for liver fibrosis–HCC transition. Graphical Abstract

Serine is crucial for tumor initiation, progression, and adaptive immunity. Metabolic pathways for serine synthesis, acquisition, and utilization in tumors and tumor-associated cells are influenced by various physiological factors and the tumor microenvironment, leading to metabolic reprogramming and amplification. Excessive serine metabolism promotes abnormal macromolecule biosynthesis, mitochondrial dysfunction, and epigenetic modifications, driving malignant transformation, proliferation, metastasis, immune suppression, and drug resistance in tumor cells. Restricting dietary serine intake or reducing the expression of serine synthetic enzymes can effectively slow tumor growth and extend patient survival. Consequently, targeting serine metabolism has emerged as a novel and promising research focus in cancer research. This paper reviews serine metabolic pathways and their roles in tumor development. It summarizes the influencing factors of serine metabolism. The article explores the significance of serine synthesis and metabolizing enzymes, along with related biomarkers, in tumor diagnosis and treatment, providing new insights for developing targeted therapies that modulate serine metabolism in cancer.

Background: The systems pharmacology approach is a target prediction model for traditional Chinese medicine and has been used increasingly in recent years. However, the accuracy of this model to other prediction models is yet to be established.Objective: To compare the systems pharmacology modelwithexperimental gene chip technology by using these models to predict targets of a traditional Chinese medicine formulain the treatment of primary liver cancer.Methods: Systems pharmacology and gene chip target predictions were performed for the traditional Chinese medicine formula ZhenzhuXiaojiTang (ZZXJT). A third square alignment was performed with molecular docking.Results: Identification of systems pharmacology accounted for 17% of targets, whilegene chip-predicted outcomes accounted for 19%.Molecular docking showed that the top ten targets (excludingcommon targets) of the system pharmacology model had better binding free energies than the gene chip model using twocommon targets as a benchmark. For both models, the core drugs predictions were more consistent than the core small molecules predictions.Conclusion:In this study, the identified targets of systems pharmacology weredissimilar to those identified by gene chip technology; whereas the core drug and small molecule predictions were similar.

Objective: This study aimed to elucidate the effects of Hederagenin (HG) on hepatocellular carcinoma (HCC) and explore its potential molecular mechanisms. Materials and methods: Virtual screening was employed to identify potential targets within core pathways of liver cancer and to analyze the possible mechanisms of HG. CCK-8 assays were used to assess the viability of HCC cells, while Hoechst 33342/PI staining was utilized to evaluate apoptosis. The migration and invasion abilities of HCC cells were examined using Transwell and scratch assays, and single-cell cloning ability was assessed via colony formation assays. Subsequent qRT-PCR was conducted to determine the mRNA expression levels of FOXO1 and FOXO6 following HG treatment. Western blot (WB) analysis was employed to measure the protein expression levels of IGF1R, FOXO1, FOXO6, MMP2, MMP9, and VEGFA, as well as the phosphorylation status of FOXO1 Ser249. Results: Virtual screening indicated that HG might exert antitumor effects through the FOXO signaling pathway. Experimental results demonstrated that HG induces apoptosis in a dose-dependent manner and inhibits the proliferation, migration, invasion, and single-cell cloning ability of HCC cells. After HG treatment, FOXO1 expression was upregulated, while the expression levels of IGF1R, phosphorylated FOXO1 Ser249, MMP2, MMP9, and VEGFA were downregulated. Conclusion: In summary, our study is the first to demonstrate that HG regulates the phosphorylation of FOXO1, affecting the proliferation, migration, and invasion of HCC cells. The findings suggest that HG can inhibit the migration of HCC cells in vitro. The data indicate that HG-mediated targeting of the FOXO1/FOXO6 pathway holds promise as a novel therapeutic approach.