Advances in cancer biology - metastasis最新文献

{"title":"Plasma proteomics reveals stage-specific EMT-linked signals: NAMPT in early and complement in advanced colorectal cancer","authors":"Raajesh Anand Natarajan ,&nbsp;Siva Kaliyamoorthy ,&nbsp;Vinoth Boopathi ,&nbsp;Jawahar Ramasamy ,&nbsp;Ravikumar Sambandam","doi":"10.1016/j.adcanc.2025.100165","DOIUrl":"10.1016/j.adcanc.2025.100165","url":null,"abstract":"<div><div>Epithelial–mesenchymal transition (EMT) plays a dual role in driving both metastatic progression and therapy resistance in colorectal cancer (CRC). To identify systemic EMT-related signals across disease stages, we performed stage-specific plasma proteomics in treatment-naïve CRC patients from an Asia–Pacific (APAC)-representative discovery cohort in India. EMT-associated proteins were curated using FANTOM5 and validated through MSigDB enrichment, with protein interaction networks constructed via STRING and GeneMANIA. We developed an EMT Progression and Resistance Index (EPRI) that integrates literature support, stage specificity, and clinical trial relevance to prioritize clinically meaningful effectors. EPRI identified NAMPT as a central hub enriched in Stage I plasma, consistent with metabolic priming via NAD⁺ biosynthesis. A NAMPT-centered subnetwork revealed stage-dependent interactions spanning complement and metabolic pathways, implicating systemic redox remodeling and PI3K/Akt signaling in EMT-driven dissemination and 5-FU/FOLFOX resistance. In later stages (III–IV), plasma signatures consolidated into complement pathway activation (notably elevated C4A/B and CR1), reflecting immune remodeling and metastatic fixation. These stage-resolved plasma signatures—ranging from NAMPT-linked metabolic priming to complement-driven EMT stabilization—offer a noninvasive framework for monitoring EMT-associated resistance and metastasis. To our knowledge, NAMPT has not previously been examined within EMT-focused plasma proteomics in CRC, highlighting the novelty of this approach while aligning with recent reports linking NAMPT to EMT, stemness, and drug resistance across cancers. The rising incidence of early-onset CRC (EOCRC), particularly in APAC populations, underscores the urgency of validating these plasma signatures in larger, longitudinal, and molecularly stratified cohorts. Together, this discovery-phase study provides regionally grounded yet globally relevant insights into EMT-linked progression and therapeutic resistance, warranting validation in expanded, longitudinal cohorts.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"16 ","pages":"Article 100165"},"PeriodicalIF":3.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145925281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combining mitochondrial morphology and cellular metabolism measurements improves colorectal cancer cell classification","authors":"Sophie Charrasse ,&nbsp;Daouda Abba Moussa ,&nbsp;Titouan Poquillon ,&nbsp;Charlotte Saint-Omer ,&nbsp;Manuela Pastore ,&nbsp;Christelle Reynes ,&nbsp;Benoit Bordignon ,&nbsp;Pierre Roux ,&nbsp;Richard E. Frye ,&nbsp;Abdel Aouacheria","doi":"10.1016/j.adcanc.2026.100175","DOIUrl":"10.1016/j.adcanc.2026.100175","url":null,"abstract":"<div><h3>Background</h3><div>In many diseases, including cancer, the number, distribution and shape of mitochondria are affected. Under stress conditions and in tumor cells, changes in cellular, nuclear and mitochondrial morphology are frequently observed. Mitochondria are responsible for energy production and metabolic reprogramming is recognized as a hallmark of cancer, including colorectal cancer (CRC), the third most common and second most deadly cancer worldwide. CRC is a heterogeneous disease, with each subtype exhibiting distinct molecular features that lead to diverse clinical outcomes. The relationship between mitochondrial morphology, metabolic status, and CRC progression has not yet been formally investigated. Here, we sought to determine whether quantitative imaging of mitochondrial shapes, in addition to metabolic measurements, could provide useful information for CRC subtyping.</div></div><div><h3>Methods</h3><div>We recently developed a novel wet-and-dry imaging pipeline (MITOMATICS) that enables the quantitative measurement of a wide range of mitochondrial shapes in their native cellular environment using high-content confocal microscopy screening. This automated pipeline, which includes statistical tests as well as supervised and unsupervised machine learning tools for analysis and visualization, was applied to monitor mitochondrial morphology in a cellular model of colon cancer progression consisting of various CRC cell lines along with paired non-tumoral cell lines. The metabolic phenotype of the multiple cell subsets was also determined in order to draw inter-assay comparisons.</div></div><div><h3>Results</h3><div>We observed that mitochondria in CRC cells were swollen and formed a fragmented network, whereas in their non-tumor counterparts, mitochondria were found to be elongated and organized into a complex branched network. Statistical analysis confirmed a clear separation between normal and CRC cells, as well as among the various CRC subtypes, based on mitochondrial morphology. In addition, our results showed that both glycolysis and OXPHOS increased as a function of CRC progression, with each tumor cell line displaying a specific metabolic signature. Interestingly, combining both types of mito-signatures improved classification accuracy.</div></div><div><h3>Conclusion</h3><div>Integration of mitochondrial shape phenotyping and metabolic profiling improves CRC cancer cell classification and could provide a novel type of biomarker for CRC screening and therapeutic decision-making.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"16 ","pages":"Article 100175"},"PeriodicalIF":3.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146173406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative transcriptomic analysis of WNT/TGFβ-driven EMT pathways and drug-gene interaction networks in epithelial ovarian cancer","authors":"Roozbeh Heidarzadehpilehrood ,&nbsp;King-Hwa Ling ,&nbsp;Habibah Abdul Hamid","doi":"10.1016/j.adcanc.2026.100178","DOIUrl":"10.1016/j.adcanc.2026.100178","url":null,"abstract":"<div><h3>Background</h3><div>Epithelial ovarian cancer (EOC) remains a lethal malignancy, and epithelial-mesenchymal transition (EMT) is a key driver of invasion, metastasis, and treatment resistance. Robust EMT-centered biomarkers in EOC are still lacking. We aimed to identify consensus EMT-related mRNA-miRNA signatures and drug-gene interactions across independent cohorts.</div></div><div><h3>Methods</h3><div>Three mRNA and one miRNA GEO datasets were analyzed. Differentially expressed genes (DEGs) were identified with limma and combined meta-analytically; consensus DEGs were directionally concordant with FDR &lt;0.05. EMT involvement was evaluated using Hallmark EMT enrichment and correlations with EMTome-derived epithelial and mesenchymal scores in TCGA-OV. Functional enrichment, protein–protein interaction networks, hub genes, Human Protein Atlas validation, drug–gene interactions, and miRNA prediction and validation were integrated.</div></div><div><h3>Results</h3><div>We identified 528 consensus DEGs (131 up-regulated, 397 down-regulated) in EOC versus normal ovary. Up-regulated genes were enriched for EMT, extracellular matrix organization, and WNT/TGFβ/BMP signaling, whereas down-regulated genes involved signal transduction and cell-cell communication. Seventeen EMT-related genes, including NT5E, VIM, GAS1, and WNT5A, showed strong mesenchymal associations. Ten hub genes (AURKA, BIRC5, CDK1, EZH2, HMMR, IQGAP3, BCL2, DCN, NT5E, PGR) were consistently dysregulated, associated with poorer survival, and supported by protein-level differences. Integration with miRNA data highlighted ten EMT-related miRNAs, several with good diagnostic performance (AUC ≥0.80). Eight clinically relevant drug-gene pairs, including alisertib (AURKA) and venetoclax (BCL2), were prioritized.</div></div><div><h3>Conclusions</h3><div>This EMT-focused integrative analysis defines coherent mRNA-miRNA-drug axes in EOC. The identified EMT-regulatory modules provide candidate diagnostic and prognostic biomarkers and pathway-based therapeutic hypotheses that warrant validation in independent cohorts and functional models.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"16 ","pages":"Article 100178"},"PeriodicalIF":3.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146173407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mathematical modeling of breast cancer: Analyzing immune-chemotherapy interactions and sensitivity to key parameters","authors":"Hossein Gholami ,&nbsp;Mortaza Gachpazan ,&nbsp;Majid Erfanian ,&nbsp;Malihe Hasanzadeh","doi":"10.1016/j.adcanc.2026.100179","DOIUrl":"10.1016/j.adcanc.2026.100179","url":null,"abstract":"<div><div>In this study, we develop a biologically informed mathematical model of breast cancer that integrates key tumor, cytokine, and immune-cell interactions. To balance mechanistic detail with computational efficiency, a stepwise modeling strategy is adopted. In the first phase, the dynamics of two major cytokines, Interleukin-2, (IL-2) and Interferon-<span><math><mi>γ</mi></math></span> (IFN-<span><math><mi>γ</mi></math></span>), are formulated together with their regulatory effects on tumor cells. Simulations show that cytokine activity alone is insufficient to control tumor progression. Motivated by this result, the model is expanded to incorporate essential immune cell populations, including natural killer (NK) cells, CD4<span><math><msup><mrow></mrow><mrow><mo>+</mo></mrow></msup></math></span> helper T cells, and CD8<span><math><msup><mrow></mrow><mrow><mo>+</mo></mrow></msup></math></span> cytotoxic T cells, with their interactions described through nonlinear feedback mechanisms such as Michaelis–Menten kinetics. Unlike classical compartmental models that treat cytokines or chemotherapy as external factors, the proposed framework introduces a novel two-phase cytokine–immune structure that mechanistically bridges molecular and cellular scales within a unified system. Despite this enhanced coupling, the immune response alone fails to eliminate tumor cells for realistic initial tumor burdens. To overcome this limitation, a constant-dose chemotherapy component is incorporated and solved using the non-standard finite difference (NSFD) method. The combined immune–chemotherapy model demonstrates complete tumor clearance even for an initial tumor size of <span><math><mrow><mn>1</mn><msup><mrow><mn>0</mn></mrow><mrow><mn>9</mn></mrow></msup></mrow></math></span> cells. Finally, sensitivity analysis identifies <span><math><msub><mrow><mi>Q</mi></mrow><mrow><mi>t</mi></mrow></msub></math></span> (chemotherapy-induced tumor cell death rate) and <span><math><msub><mrow><mi>r</mi></mrow><mrow><mi>t</mi></mrow></msub></math></span> (tumor growth rate) as the most influential parameters, offering valuable guidance for optimizing treatment strategies. It should be noted that model validation is performed using rescaled, population-averaged tumor growth data, and therefore the reported fit supports reproduction of population-level trends rather than individualized patient-specific prediction.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"16 ","pages":"Article 100179"},"PeriodicalIF":3.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147384856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repurposing statins in combination therapy for effective ablation of metastatic breast cancer","authors":"Rifat Aara ,&nbsp;Neeha Sinai Borker ,&nbsp;Jyothilakshmi Sajimon ,&nbsp;Seemadri Subhadarshini ,&nbsp;Snijesh VP ,&nbsp;Vidya P. Nimbalkar ,&nbsp;Manju Moorthy ,&nbsp;Archana P. Thankamony ,&nbsp;Athul Krishnan R ,&nbsp;Mohit Kumar Jolly ,&nbsp;Jyothi S. Prabhu ,&nbsp;Radhika Nair","doi":"10.1016/j.adcanc.2025.100166","DOIUrl":"10.1016/j.adcanc.2025.100166","url":null,"abstract":"<div><div>Metastatic breast cancer (mBC) remains an incurable disease with limited treatment options, highlighting the need for novel therapeutic approaches. The eventual development of resistance to commonly used regimens leading to relapse suggested the presence of intrinsically resistant heterogeneous cell populations. Our previous work identified heterogeneous metastatic tumor cell populations with distinct molecular characteristics driven by MACC1 (Metastasis Associated Colon Cancer 1), which is a key driver of metastasis and therapeutic resistance in multiple solid cancers, including breast cancer. We demonstrated that lovastatin (transcriptional inhibitor of MACC1) treatment ablated the metastatic cells through Macc1 downregulation. Building on this foundation, we evaluated the efficacy of lovastatin in lung metastases and elucidated its regulatory pathways in mBC.</div><div>Spatial transcriptomics on an Indian breast cancer patient cohort revealed heterogeneous MACC1 expression across tumors, which correlated with aggressive clinical features. Heterogeneous tumor cells [bulk tumor (Bulk), primary tumor (T1), lung-specific metastatic (L1) cells] were characterized from a metastatic murine model, with L1 showing the highest proliferation rate and MACC1 expression. Lovastatin treatment significantly downregulated MACC1 expression in L1 cells resulting in inhibition of key metastatic phenotypes like proliferation and migration, as well as altered cell type-specific gene expression of programmes like EMT and dormancy, with protein–ligand docking simulations with Sp1, indicating a potential transcriptional regulatory mechanism. Finally, we explored the therapeutic efficacy of lovastatin in combination with chemotherapy and demonstrated that lovastatin effectively ablated chemoresistant tumor cells in mBC. The translational implications of this research could identify patient subgroups that may benefit from statin–chemotherapy combinations and support the repurposing of statins as cost-effective adjuvant therapies for mBC.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"16 ","pages":"Article 100166"},"PeriodicalIF":3.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145618489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heat stress therapies for head and neck squamous cell carcinoma: Bibliometrics retrospective view","authors":"Yuhao Guo ,&nbsp;Chenzhou Wu ,&nbsp;Pengfei Li ,&nbsp;Haitao He ,&nbsp;Longjiang Li","doi":"10.1016/j.adcanc.2026.100174","DOIUrl":"10.1016/j.adcanc.2026.100174","url":null,"abstract":"<div><div>Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer globally, with a 5-year survival rate of approximately 46 %. Although surgery, radiotherapy, and chemotherapy effectively treat HNSCC, they often cause severe side effects, including mucositis, salivary gland damage, osteonecrosis of the jaw, and other persistent adverse events. In contrast, heat stress-based therapies provide a precise, minimally invasive, and effective alternative.</div><div>This study aimed to perform an in-depth bibliometric analysis of heat stress-based therapies for HNSCC over the past three decades, with a focus on identifying key trends, innovations, and future challenges, particularly in integrating nanotechnology with molecular therapies. Major research areas include heat shock protein (HSP) metastatic phenotypes, functions, and mechanisms; innovative detection methods and research tools; emerging therapies and pharmaceutical developments; and nanomaterials combined with photothermal therapy for HNSCC treatment. The findings of this study highlight HSPs and nanomaterials as hotspot areas of recent investigation. Additional exploration was done regarding novel detection methods and treatment strategies, especially in the context of precision medicine and minimally invasive approaches. This study offers valuable insights into future HNSCC treatment directions and essential guidance for researchers and clinicians in the field.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"16 ","pages":"Article 100174"},"PeriodicalIF":3.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146173405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting epithelial-to-mesenchymal transition of cancer cells by sulfated glycans from marine algae","authors":"Olesya S. Malyarenko ,&nbsp;Anna O. Kravchenko ,&nbsp;Valery R. Druzhinina ,&nbsp;Rohit Gundamaraju ,&nbsp;Svetlana P. Ermakova ,&nbsp;Ranga Rao Ambati","doi":"10.1016/j.adcanc.2026.100172","DOIUrl":"10.1016/j.adcanc.2026.100172","url":null,"abstract":"<div><div>Epithelial-mesenchymal transition (EMT) represents a process whereby an epithelial cell undergoes a series of alterations, acquiring the morphological and functional characteristics of a mesenchymal cell. EMT plays a significant role in the progression of cancerous cells, including metastasis, tumor heterogeneity and drug resistance. Despite the identification of multiple molecular pathways implicated in the regulation of tumor EMT, no specific treatment has been developed to target this process. The bioactive compounds derived from seaweeds represent a significant area of research interest, given their potential therapeutic applications in a range of diseases. Sulfated glycans, derived from brown, red, and green algae, as well as their derivatives, have demonstrated anticancer activity <em>in vitro</em>, <em>in vivo</em>, and under preclinical conditions. This review summarizes the key and pivotal aspects of the use of fucoidans, carrageenans, and ulvans derived from brown, red, and green algae, respectively, and their derivatives, in the modulation of pathological EMT or its deleterious effects through the modulation of various cellular signal transduction pathways, both <em>in vitro</em> and <em>in vivo</em>. The objective of this review is to elucidate the molecular mechanisms underlying the antitumor effects of sulfated seaweed's glycans and to provide insights into the relevance of individual polysaccharides in influencing tumor EMT, which may contribute to the development of new alternative cancer treatment options.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"16 ","pages":"Article 100172"},"PeriodicalIF":3.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miRNA-4722-3p targets GGT5 and inhibits gastric cancer cell progression via the PI3K/AKT-MAPK-MMPs signaling pathway","authors":"Xuxia Ye ,&nbsp;Fanfan Yang ,&nbsp;Hui Huang ,&nbsp;Mengli Wu ,&nbsp;Jin Chen ,&nbsp;Bin Xu ,&nbsp;Jian Xu","doi":"10.1016/j.adcanc.2026.100170","DOIUrl":"10.1016/j.adcanc.2026.100170","url":null,"abstract":"<div><div>Gastric cancer (GC) is a common gastrointestinal malignancy, with more than one million new cases diagnosed each year. Identifying biomarkers for early diagnosis and prognosis is crucial to improving clinical outcomes. However, existing biomarkers lack sufficient sensitivity and specificity. Gamma-glutamyltransferases (GGTs) are a family of enzymes involved in glutathione metabolism and cancer progression, and recent studies have suggested their potential as tumor markers. Among them, GGT5 (Gamma-glutamyltransferase 5) has been reported to play oncogenic roles in gastrointestinal cancers.This study aims to explore the regulatory relationship between miRNA-4722-3p and GGT5 and its impact on GC progression, evaluating the potential of miRNA-4722-3p as a diagnostic biomarker for GC. Bioinformatics tools, including TargetScan, miRWalk, and miRDB, were used to predict miRNAs that bind to the 3’ untranslated region (UTR) of GGT5. miRNA-4722-3p was selected due to its lowest binding free energy and was validated through dual-luciferase reporter assays. RT-qPCR and Western blotting confirmed that miRNA-4722-3p directly targets and inhibits GGT5 expression in GC cells. Functional assays demonstrated that miRNA-4722-3p upregulation significantly suppressed GC cell proliferation and migration, whereas its downregulation enhanced these processes. Furthermore, miRNA-4722-3p inhibited GGT5 expression through the PI3K/AKT-MAPK-MMPs signaling pathway, reinforcing its suppressive effects. Overall, miRNA-4722-3p and GGT5 may serve as promising biomarkers for the early diagnosis and targeted therapy of gastric cancer.</div></div><div><h3>Summary</h3><div>Bioinformatics and experiments identify miR-4722-3p as a gastric cancer biomarker. It suppresses tumor growth/metastasis by targeting oncogene GGT5 and inhibiting the PI3K/AKT-MAPK-MMPs pathway, revealing its tumor-suppressive role and offering a novel therapeutic target.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"16 ","pages":"Article 100170"},"PeriodicalIF":3.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the mechanism of Jianpi Guchang recipe and its compound: Inhibition liver metastasis in colorectal carcinoma through regulation of the bile acid-FXR-FGF19 axis","authors":"Cunya Li ,&nbsp;Pantong Wu ,&nbsp;Zhonghua Wu ,&nbsp;Jian Chen ,&nbsp;Zhiying Wang ,&nbsp;Zhixian Zhong ,&nbsp;Yi Zhong ,&nbsp;Shujuan Fu","doi":"10.1016/j.adcanc.2026.100180","DOIUrl":"10.1016/j.adcanc.2026.100180","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the main mechanism by which Jianpi Guchang recipe (JPGC) prevents liver metastasis in patients with intestinal cancer and explain the related microbiological changes that regulate bile acid metabolism.</div></div><div><h3>Methods</h3><div>To explore the effects of JPGC and its Compound on various phenotypes of colon cancer cells, the expression of FXR-related upstream and downstream genes and proteins was assessed by RT‒qPCR. A mouse model of intestinal cancer liver metastasis was established, and the effects of the JPGC on basic conditions, tumor growth, serum bile acid levels, inflammation levels and the expression of bile acid metabolism-FXR-FGF15 axis-related proteins were analyzed.</div></div><div><h3>Results</h3><div>1. JPGC and its Compound effectively inhibited the proliferation and migration of colon cancer cells. 2. JPGC significantly upregulated the expression of the bile acid metabolism-related genes FXR and FGF19 in colon cancer cells. 3. JPGC improved the activity state, increased body weight, reduced liver metastasis, and decreased serum bile acid and inflammatory factor levels in mice with colon cancer liver metastasis. 4. JPGC upregulated E-cadherin expression in the intestine, downregulated MMP-2 expression in the liver, and upregulated FXR and FGF-19/15 expression in the intestine and liver.</div></div><div><h3>Conclusion</h3><div>The mechanism by which JPGC inhibits liver metastasis in patients with colorectal cancer is closely related to the regulation of bile acid metabolism. JPGC plays an anti-liver metastasis role by stabilizing bile acid levels, mainly by promoting FXR expression and inhibiting inflammatory reactions.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"16 ","pages":"Article 100180"},"PeriodicalIF":3.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147384861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-breast cancer effects of free and nanocarrier-loaded salinomycin and doxorubicin","authors":"Zohreh Amiri ,&nbsp;Mehdi Forouzandeh Moghadam ,&nbsp;Zahra Sadat Hashemi ,&nbsp;Majid Sadeghizadeh ,&nbsp;Abdolah Razi","doi":"10.1016/j.adcanc.2025.100168","DOIUrl":"10.1016/j.adcanc.2025.100168","url":null,"abstract":"<div><h3>Introductio</h3><div>n: Salinomycin (SAL) and doxorubicin (DOX) have previously garnered much attention as anticancer drugs. However, their encapsulation within a nanocarrier dendrosome and their possible synergistic effect have not been reported, which we aim to address.</div></div><div><h3>Methods</h3><div>SAL and DOX were loaded into the produced OA400 nanocarrier. Then, their effects on cell viability, apoptosis, migration, and invasion were analyzed in MDA-MB-231 and MCF-7 cells. The evaluations were conducted using MTT, flow cytometry, scratch, and Matrigel tests. The treatments were performed with encapsulated and free forms of the individual drugs, and in combination. The miRNAs Let-7, miR-21, miR-10b, and miR-128 expression was assessed by qRT-PCR to evaluate the cellular effects of the treatments.</div></div><div><h3>Results</h3><div>The results showed that the combination of free SAL and DOX and the combination of SAL and DOX loaded in OA400 were more effective than their treatment as singular drugs in the inhibition of proliferation and induction of apoptosis. The expression of miRNAs, miR-21 and miR-10b, the most important tumor miRNAs, was decreased, and the expression of Let-7, an inhibitor of tumor growth, was increased. However, miR-128 expression didn't change significantly.</div></div><div><h3>Conclusion</h3><div>The nanocarrier OA400 provides a potential strategy for targeted delivery of SAL and DOX, providing a sustained release profile. Moreover, combined administration of these drugs showed a synergistic anticancer activity, which could be deemed as an effective anti-cancer therapy against breast cancer. Despite the obtained promising results, further <em>in vivo</em> studies would shed light on the true potential of this strategy.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"16 ","pages":"Article 100168"},"PeriodicalIF":3.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}