The purpose of this study is to investigate the main active components and potential mechanisms of action of Yiyi Fuzi Baijiang powder against colorectal cancer by network pharmacology and molecular docking. Firstly, the TCMSP database was used to search for the active ingredients and targets of Yiyi Fuzi Baijiang powder, and colorectal cancer disease genes were collected through GeneCards and DisGeNET database. The intersection genes between Yiyi Fuzi Baijiang powder and colorectal cancer were then found using the web program Venny 2.1.0. Next, a protein interaction network was constructed using the STRING database, and Cytoscape 3.7.1 was used to screen and display the main targets. The David database uses functional Gene Ontology (GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis to examine key targets. To filter the primary active components, an ”active ingredient-target-pathway” network was built using Cytoscape 3.7.1. Finally, AutoDockTool and PyMOL were used to validate molecular docking. Yiyi Fuzi Baijiang powder and CRC yield 176 intersection targets. Quercetin, luteolin,kaempferol, stigmasterol, and β-sitosterol are the main active substances, whereas HSP90AA1, TP53, JUN, AKT1, and MAPK1 are the main targets. Yiyi Fuzi Baijiang powder may influence the PI3K-Akt signaling pathway, TNF signaling route, and IL-17 signaling pathway, which are involved in transcription, gene expression, apoptosis and proliferation regulation, among other biological processes, according to GO and KEGG enrichment analyses. The results of the molecular docking demonstrated that all of the major targets could be strongly bound by the core active chemicals in Yiyi Fuzi Baijiang powder. By simultaneously controlling several active components’ target genes and associated signaling pathways, Yiyi Fuzi Baijiang powder may slow the advancement of colorectal cancer by controlling apoptosis, proliferation, and the binding of proteins and enzymes.

Several studies have demonstrated the positive impact of non-pharmacological Traditional Chinese Medicine (TCM) therapies on pain, fatigue, sleep quality, and quality of life in cancer survivors. However, no research has compared the effectiveness of these therapies. This study aims to compare various interventions and identify the most effective non-pharmacological TCM therapies to provide evidence-based recommendations for cancer survivors. A systematic search was conducted in PubMed, Embase, Web of Science, CNKI, and Wanfang Data. RCTs investigating the effects of Taichi, Qigong, acupuncture, acupressure, TCM emotional therapy, and mixed therapies as interventions for cancer survivors were screened was conducted. Data from the creation of the database to February 2025 were included. Two independent reviewers evaluated the study quality. A Bayesian Network Meta-analysis was conducted to carry out a random effects model. Seventy-one RCTs involving 6473 patients were included in the analysis. Network meta-analysis showed significance for all five intervention therapies in pain control in cancer patients. The best efficacy was observed for acupressure (SMD=-1.1 [-1.55, -0.66]) and Taichi/Qigong (SMD=-1.08[-1.64, -0.53]), followed by TCM emotional therapy (SMD=-0.93 [-1.42, -0.44]) and acupuncture (SMD=-0.54 [-0.93, -0.15]), with the latter showing comparatively lower efficacy. None of the interventions demonstrated superior efficacy in improving fatigue compared to the control group. Mixed therapies (SMD=-1.36[-2.56, -0.28]) demonstrated the greatest effect in improving sleep quality. Taichi/Qigong (SMD=1.87 [0.96, 2.83]) demonstrated certain advantages in improving quality of life. However, acupuncture and TCM emotional therapy had no significant effect on sleep quality or overall quality of life. The evidence from this study suggests that acupressure and Taichi/Qigong are recommended as the most effective therapies for pain relief and quality of life improvement, respectively. The efficacy of these therapies for fatigue remains inconclusive. However, due to the limited number of included studies and the high risk of bias, these results should be interpreted with caution. Future studies should include more rigorously designed high-quality randomized controlled trials to confirm their long-term efficacy and safety. PROSPERO CRD42024601976.

Objective: Evaluate the therapeutic efficacy and safety of Traditional Chinese Medicine (TCM) in patients with primary liver cancer (PLC) receiving targeted therapy. Methods: We conducted a comprehensive search of databases. The search scope covered the period from the establishment of the databases to April 2025. We included 49 randomized controlled trials (RCTs) evaluating targeted therapy for primary liver cancer with TCM. Efficacy and safety outcomes were assessed using risk ratios (RR), standardized mean differences (SMD), and their 95% confidence intervals (CI). Results: Targeted therapy for liver cancer patients who received TCM treatment showed improvements in objective response rate (ORR) (RR, 1.49 [1.33-1.66], P < 0.0001), disease control rate (DCR) (RR, 1.32 [1.25,1.40], P < 0.0001), the 1-year survival (RR, 1.50 [1.20,1.88]; P = 0.0004) and Karnofsky Performance Status (KPS) (SMD, 1.34 [0.86,1.81]; P < 0.0001), and can reduce the incidence of adverse events, as well as to some extent decrease the production of tumor markers and related inflammatory factors. Conclusion: TCM enhances the efficacy and safety of targeted therapy in PLC, offering superior clinical outcomes with fewer adverse effects. These findings support its potential integration into standard treatment protocols. Systematic review registration: https://www.crd.york.ac.uk/prospero/ , identifier CRD420251055085.

Previous studies have identified an association between per- and polyfluoroalkyl substances (PFAS) and the occurrence of intrahepatic cholangiocarcinoma (ICC), but the specific mechanisms remain unclear. This study aims to analyze the toxicological mechanisms of PFAS, particularly perfluoroctanoic acid (PFOA) and perfluorooctane sulfonate (), on ICC through network toxicology and bioinformatics. Relevant targets for PFOS and PFOA were retrieved from the CTD, ChEMBL, and Super-PRED databases. Targets related to ICC were gathered from the GeneCards, NCBI, and OMIM databases. Common targets between ICC and PFOS, PFOA were identified and subjected to median filtering in CytoHubba to select core targets, which were then analyzed for protein–protein interaction using the STRING database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed on core targets to elucidate the biological processes affected by PFAS in ICC. The intersection of the targets for ICC and those from PFOS/PFOA was compared with the differentially expressed genes in ICC from the TCGA database. LASSO regression was applied to filter prediction targets, and bioinformatics analysis was conducted to assess the differential expression of these targets in ICC, constructing a risk assessment model. Molecular docking was utilized to evaluate the binding affinity of PFOA and PFOS to the predicted targets. A total of 1,838 and 2,616 targets were predicted for PFOA and PFOS, respectively; whereas, for ICC, 2,044 targets were identified, with 345 and 459 common targets for PFOA and PFOS, respectively. GO and KEGG enrichment analyses revealed that these processes were primarily associated with biological functions such as cell proliferation and apoptosis, potentially mediated by the PI3K-Akt and HIF-1 signaling pathways. The integrated analysis of differentially expressed genes from the TCGA database and the intersection of targets from PFOA/PFOS with those from ICC yielded five core genes (TP53, ESR1, CDH1, BCL2, and MMP9) that formed an ICC prognostic score with robust predictive capability for survival, classifying ICC patients into high-risk and low-risk groups (p < 0.05). Molecular docking simulations demonstrated strong binding affinities between PFAS and these core targets, supporting their potential roles in PFAS-induced ICC development. This study explores the potential key mechanisms underlying PFAS-induced ICC and highlights core biomarkers that could serve as therapeutic targets. These results are expected to offer novel perspectives on strategies for the prevention and treatment of ICC.

Background: Previous studies indicate that Acalypha australis L. (AAL), a traditional Miao medicine, effectively treats colitis, but its anti-tumor effects on colorectal cancer (CRC) are unclear. Objective: This study aims to investigate the anticancer effects of ethanol extracts of Acalypha australis L. (EEAL) against CRC and elucidate their potential mechanisms of action. Methods: This study first employed ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) to analyze the chemical components of EEAL and utilized databases like TCMSP to identify potential anticancer compounds against CRC. Network pharmacology was then used to predict the mechanisms and targets of EEAL in CRC treatment. The effects of EEAL on the proliferation of LOVO and HCT116 CRC cells were assessed using CCK-8 assays and colony formation experiments. Changes in membrane integrity were measured with CM-Dil staining, along with mitochondrial membrane potential and intracellular reactive oxygen species (ROS) levels. The extent of autophagy after treatment was evaluated with transmission electron microscopy and Lyso-Tracker staining to observe autophagosome (ASS) expression. Finally, Western blot (WB) analysis was performed to assess the expression of relevant proteins and investigate the potential anticancer mechanisms of EEAL against CRC. Results: A total of 30 candidate components with potential anticancer activity against CRC were identified from EEAL. Network pharmacology analysis suggested that EEAL may regulate oxidative stress in CRC treatment through the AKT/mTOR/HIF-1 pathway. Cellular experiments demonstrated that EEAL significantly inhibited the proliferation and colony formation ability of LOVO and HCT116 CRC cells. Further studies revealed that EEAL not only decreased mitochondrial membrane potential and increased intracellular ROS levels but also induced significant accumulation of autophagic lysosomes and compromised membrane integrity. Western blot analysis showed that EEAL decreased the protein expression of AKT, P-mTOR, and HIF-1, while upregulating the expression of the autophagy marker LC3B. Conclusion: This study demonstrates that EEAL exerts its anticancer effects against CRC by inhibiting the AKT/mTOR/HIF-1 pathway, leading to oxidative stress and mitochondrial dysfunction, which subsequently triggers excessive autophagy and compromises cell membrane integrity.

Gehua Hugan Gao (GHHGG) is a traditional Chinese medicine paste that is chiefly used to treat liver cancer. However, the potential impact of GHHGG on liver cancer remains unclear. We explored how GHHGG treats liver cancer using bioinformatics, network pharmacology, and molecular docking. Network pharmacology included GHHGG active ingredients, predicted targets, predicted targets for liver cancer, and differential gene collection. A protein-protein interaction network was constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins database, and crucial targets were ranked according to their degree values. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses of liver cancer targets were followed by survival, differential analysis, and molecular docking. Venn diagrams show 123 predicted GHHGG targets for the treatment of hepatocellular carcinoma (HCC). Enrichment analysis showed that GHHGG treats HCC through multiple targets and pathways. We also found that estrogen receptor 1, cytochrome P450 3A4, cyclin-dependent kinase 4, type IIA topoisomerase, aurora kinase A, and cyclin E1 targets were closely associated with HCC development through survival and differential analyses. Molecular docking confirmed GHHGG’s strong affinity for liver cancer targets. This study helps us understand GHHGG ingredients and targets for liver cancer treatment. To a certain extent, the molecular mechanism of GHHGG in the treatment of liver cancer has been elucidated, thus providing a theoretical basis.