Medical Oncology最新文献

{"title":"Revisiting Ehrlich carcinoma in the era of precision oncology: bridging classical models with modern systems biology.","authors":"Varshini Manjunath, Rachana Rajesh Nayak, Ananth Koushik Bhujanga, Arpitha Maraliga Ramesh, Prasanna Kumar Santhekadur","doi":"10.1007/s12032-026-03452-x","DOIUrl":"10.1007/s12032-026-03452-x","url":null,"abstract":"<p><p>Ehrlich carcinoma (EC) and its ascitic form, Ehrlich ascites carcinoma (EAC), are among the oldest and most widely used experimental tumor models in cancer research. Although they have traditionally been used for anticancer drug screening, their potential to address broader aspects of aggressive tumor biology has received comparatively less attention. EC/EAC exhibits several characteristics associated with advanced malignancy, including rapid tumor growth, angiogenesis, immune dysregulation, metabolic changes, therapeutic resistance, and complex interactions between the tumor and host. These features make EC/EAC a useful complementary model for studying different aspects of tumor progression. However, research using these models has largely focused on transcriptional changes and individual signalling pathways, while post-transcriptional regulatory mechanisms remain less explored. In particular, the role of the RNA-induced silencing complex (RISC), a major component of microRNA-mediated gene regulation, is still poorly understood in EC/EAC. In this review, we discuss the major limitations of current EC/EAC research, including the limited use of multi-omics approaches, single-cell and spatial analyses, functional genomics, immune checkpoint profiling, and integrated systems-level studies. We further discuss how incorporating RISC-centered regulatory networks with emerging approaches such as CRISPR-based studies, spatial transcriptomics, and metabolic profiling could provide deeper mechanistic insights and improve the translational value of these models. Bringing together the strengths of this established tumor model with contemporary approaches in cancer biology could help reposition EC/EAC as a relevant and versatile platform for studying tumor progression and therapeutic responses.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Marine microbial arginase: a metabolic therapeutic strategy for oral squamous cell carcinoma.","authors":"R Priya, G Ragul, G Ritika, Kamala Kannan, Dhanraj Ganapathy, Sivaperumal Pitchiah","doi":"10.1007/s12032-026-03456-7","DOIUrl":"https://doi.org/10.1007/s12032-026-03456-7","url":null,"abstract":"<p><p>Oral squamous cell carcinoma (OSCC) represents a significant clinical burden, with limited advancements in metabolic-targeted therapies. Arginase is a metalloenzyme that plays an essential role in the hydrolysis of L-arginine into urea and L-ornithine. In recent years, arginase enzyme also shows promising role in therapeutic especially in anti-cancer therapy through arginine deprivation therapy (ADT). Among many tumors that are arginine-auxotrophic due to downregulation of ASS1 are hepatocellular carcinoma, melanoma, and subsets of oral cancers, and are therefore susceptible to depletion of extracellular arginine. Although recombinant human arginase has advanced to preclinical and clinical trials, issues such as immunological reactions and limited stability have sparked interest in alternative sources. Marine microorganisms, especially from deep-sea environments, are known to produce unique and stable enzymes with high catalytic efficiency and are less prone to protein denaturation. As a result of their remarkable stability in harsh conditions and variety of structures, marine microbial arginases have emerged as the top candidates for investigation. In addition to remaining active at varying pH, salinity, and temperatures, these enzymes offer a versatile platform for protein engineering and therapeutic optimisation. This review focuses on the biochemical and structural properties of arginase, compares microbial and human forms, and explores the mechanisms of its antitumor action, including tumor cell growth inhibition, angiogenesis modulation, and immune suppression within the tumor microenvironment. Additionally, it identifies developments in marine bioprospecting, combination strategies with immunotherapy, and nanoparticle-based delivery as major trends influencing future research.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vitro assessment of the free radical scavenging and cytotoxic activities of Piper betle leaf essential oil.","authors":"Parthiban Janani, Alagiri Anju, Ashok Anjana, R Dinesh Babu, Velayutham Meiyalagan","doi":"10.1007/s12032-026-03462-9","DOIUrl":"https://doi.org/10.1007/s12032-026-03462-9","url":null,"abstract":"<p><p>In traditional medicine, natural plant-based treatments have played a key role in preventing and addressing different ailments. They are also considered an important source of bioactive compounds with potential pharmacological applications. The leaves of the widely known medicinal plant Piper betle are widely utilized in traditional medicine due to their biological qualities. The bioactive compounds found in the essential oil extracted from Piper betle leaves are especially abundant and are thought to have a major role in the plant's medicinal potential. In the current study, the antioxidant and anticancer properties of essential oil extracted from Piper betle leaves were objectively evaluated using in vitro experimental methods. To thoroughly investigate the essential oil's capacity to reduce oxidative stress, its antioxidant activity was evaluated using a variety of free radical scavenging assays, such as the DPPH, Hydrogen Peroxide, Superoxide Dismutase, and ABTS assays. The anticancer activity was investigated against human oral carcinoma (KB) cell lines by assessing cytotoxicity and membrane damage. The MTT assay was performed to assess cell viability at doses between 6.25 and 100 µg/mL, with an IC₅₀ value determined to be 22.8 µg/mL, the essential oil demonstrated considerable antiproliferative activity and significant, concentration-dependent cytotoxicity against KB cells. In addition, the essential oil demonstrated pronounced antioxidant activity across all tested assays. The presence of many bioactive components with functional groups known to be important in scavenging free radicals and inhibiting cancer cells may be responsible for the reported biological activity. Overall, these findings highlight the potential of Piper betle leaf essential oil as a dual-action agent with notable anticancer and antioxidant capabilities.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging Role of the Tumor Microenvironment in the Development of Metastasis, Drug Resistance, and Molecular Targeted Strategies A Commentary.","authors":"Rashid Mir, Ajaz Ahmad Waza, Sufiyan Khan","doi":"10.1007/s12032-026-03465-6","DOIUrl":"10.1007/s12032-026-03465-6","url":null,"abstract":"<p><p>It is gradually becoming clear that cancer development represents a systems-level process that is controlled by dynamic and reciprocal interactions between the tumor microenvironment (TME) and malignant cells. The TME does not act as a passive scaffold but active regulation of tumor initiation, growth, metastatic dissemination, immune evasion and therapeutic resistance in terms of coordinated metabolic, signaling and immunological networks. Adaptive metabolic reprogramming and phenotypic plasticity in both cancer and stromal compartments were found in microenvironmental stressors like hypoxia, nutrient deprivation, and extracellular acidosis. The adaptations maintain invasive, cancer stem cell persistence, immune suppression and survival upon therapeutic pressure. Crosstalk between cells metabolism, exosome-based communication, and extracellular matrix reorganization all determine ecosystem-level resilience disrupting traditional cancer therapies. Within the framework of this commentary, we generalize emerging evidence that places the TME at a hub of metastasis and drug resistance, and we focus on metabolic plasticity, stromal re-programming and immune-metabolic competition. Based on the integrative multi-omics framework by Mir et al., we expand on the way genomics, transcriptomics, proteomics, metabolomics, and spatial profiling are redefining precision oncology by solving intratumoral heterogeneity and determining ecosystem-wide vulnerabilities. Lastly, we emphasize the possibilities of translational multi-omics-informed targeting of metabolic and stromal dependencies to break tumor ecosystem resilience and resulting clinical responses to be more durable. Importantly, such therapeutic concepts should be interpreted within the context of the intrinsic biological complexity of the tumor ecosystem, in which metabolic interventions may have divergent and cell-type-specific effects on malignant, stromal, and immune compartments, necessitating careful translational consideration.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative transcriptomic and network analysis elucidates the multi-target molecular mechanisms of carboplatin in melanoma.","authors":"Mobina Shahriarizade, Seyed Mehdi Ahmadi, Ali Ahmadizad Firouzjaei","doi":"10.1007/s12032-026-03460-x","DOIUrl":"https://doi.org/10.1007/s12032-026-03460-x","url":null,"abstract":"<p><p>Melanoma is an aggressive malignancy with high metastatic potential and frequent resistance to standard therapies, highlighting the need for robust biomarkers and improved mechanistic understanding of effective treatments. This study integrates transcriptomic profiling and network-based analyses to identify key regulatory genes and clarify how clinically used agents may counteract melanoma-specific molecular dysregulation. Comparative evaluation of three independent gene expression datasets yielded 194 overlapping differentially expressed genes (DEGs) enriched in pathways central to tumor progression. A protein-protein interaction network was constructed, and hub genes were prioritized using the Maximal Clique Centrality algorithm, revealing critical nodes involved in melanoma biology. Drug-gene interaction analysis via DGIdb identified carboplatin as a multi-target compound interacting with CDKN1A, BRCA1, PTEN, and AKT1. Although carboplatin, often combined with paclitaxel, is already utilized clinically for advanced or treatment-refractory melanoma, its multi-target molecular effects in relation to melanoma transcriptomic alterations remain insufficiently defined. Experimental validation in B16F0 melanoma cells demonstrated dose- and time-dependent cytotoxicity, with an IC₅₀ of approximately 17 µM at 48 h. RT-qPCR analysis showed increased expression of CDKN1A, BRCA1, and PTEN, alongside reduced AKT1 expression, indicating activation of DNA damage response pathways and reinforcement of tumor-suppressive signaling. Overall, this study identifies key molecular determinants of melanoma progression and provides mechanistic evidence explaining carboplatin's therapeutic activity through modulation of dysregulated transcriptomic hubs. The combined computational and experimental framework offers a valuable strategy for biomarker discovery and mechanistic evaluation of clinically used agents in melanoma research.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL1RAP promotes EMT and metastatic phenotypes in papillary thyroid carcinoma and is associated with PI3K/AKT signaling activation.","authors":"Yongkui Zhao, Yunlei Shao, Zhiwei Guo, Mingyue Guo","doi":"10.1007/s12032-026-03453-w","DOIUrl":"https://doi.org/10.1007/s12032-026-03453-w","url":null,"abstract":"<p><p>Although papillary thyroid carcinoma (PTC) usually follows an indolent course, lymph node metastasis and locally advanced disease remain clinically important challenges. This study evaluated interleukin-1 receptor accessory protein (IL1RAP) in PTC using pan-cancer datasets, TCGA/GEO thyroid cancer cohorts, and in vitro validation. IL1RAP was upregulated in PTC tissues and cell lines, and higher IL1RAP expression was associated with advanced pathologic stage, lymph node metastasis, extrathyroidal extension, and unfavorable prognostic indicators. Functional assays showed that IL1RAP overexpression increased PTC cell proliferation, migration, invasion, and EMT-like changes, whereas transient IL1RAP silencing produced the opposite pattern. Bioinformatic enrichment and western blot analyses indicated that these cellular effects were accompanied by increased p-AKT with minimal change in total AKT, suggesting possible involvement of PI3K/AKT-related signaling. To our knowledge, this is the first systematic analysis linking IL1RAP to EMT-associated aggressive behavior in PTC. IL1RAP may represent a candidate biomarker associated with aggressive clinicopathological features, while its diagnostic/prognostic utility and therapeutic potential require further validation.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL14-mediated FDX1 m6A methylation inhibited the proliferation of clear cell renal cell carcinoma.","authors":"Zhijie Bai, Chun Wang, Junlin Shen, Yanjie Yang, Qian Liu, Zhiqun Shang","doi":"10.1007/s12032-026-03438-9","DOIUrl":"10.1007/s12032-026-03438-9","url":null,"abstract":"<p><p>FDX1 exerts a significant influence in the process of cuproptosis by facilitating the lipoacylation of proteins and reducing copper ions to monovalent copper ions. The methyltransferase METTL14 is an enzyme that modulates the m6A methylation of RNA, which can impact the stability, translation efficiency, and degradation rate of RNA. Nevertheless, the regulatory association between METTL14 and FDX1 in kidney cancer requires further investigation. The differential expression of METTL14 and FDX1 between normal tissues and renal cancer tissues was analyzed via the GEO public database. The association between these factors and patient survival was analyzed by utilizing the TCGA public database. A correlation analysis between METTL14 and FDX1 was performed based on the TCGA database. The findings were validated through RT - qPCR, Western blot, and immunohistochemistry assays. By using SRAMP tools and m6A correlation experiments, the study elucidated the reason for the decreased expression of FDX1 in renal cancer cells. In vivo and in vitro experiments were conducted to verify the regulatory effect of METTL14 on FDX1. In clear cell renal cell carcinoma (ccRCC), METTL14 and FDX1 exhibit downregulation and are correlated with a poor prognosis among ccRCC patients. METTL14 augments the expression of FDX1 by enhancing the stability of the FDX1 messenger RNA. METTL14 upregulates FDX1 expression and consequently enhances cuproptosis in ccRCC cells. Methyltransferase METTL14 preserves the stability of FDX1 messenger RNA via m6A modification of FDX1 messenger RNA and acts as a crucial mediator of cuproptosis. Nevertheless, in clear cell renal cell carcinoma (ccRCC), the level of cuproptosis declines as a result of the diminished expression of these two factors, and the proliferation capabilities of ccRCC cells are augmented.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The neolignan Miliusin B inhibits cell migration and promotes apoptotic cell death in cervical cancer cell line HeLa.","authors":"Roongtiwa Srisuphan, Kanok-On Rayanil, Supusson Pengnam, Pawaris Wongprayoon, Purin Charoensuksai","doi":"10.1007/s12032-026-03457-6","DOIUrl":"https://doi.org/10.1007/s12032-026-03457-6","url":null,"abstract":"<p><p>Previously, we reported the discovery, chemical characterization, and preliminary anticancer activity of Miliusin B (MB), a natural neolignan from Miliusa sessilis, demonstrating cytotoxicity and selectivity against the human cervical cancer cell line HeLa. In the present study, we further investigated the underlying anticancer mechanisms of MB. Consistent with our earlier findings, MB exhibited sub-micromolar cytotoxicity toward HeLa cells with >60-fold selectivity relative to non-cancerous controls. Mechanistic analyses revealed that cytotoxic concentrations of MB (5 µM) induced G2/M cell-cycle arrest and activated apoptotic pathways, as evidenced by caspase-9, caspase-3 and PARP cleavage. In addition, MB significantly impaired HeLa cell migration at sub-toxic concentrations (≤ 0.5 µM). Its efficacy was further validated using a three-dimensional spheroid model, where MB suppressed spheroid growth at 0.5 and 5 µM. Finally, combinatorial assays with standard cisplatin (Cis)-based cervical cancer chemotherapeutics (Cis monotherapy and Cis doublet regimens) demonstrated that MB enhanced the anti-proliferative effects of all treatments tested. Collectively, these findings highlight MB as a promising selective cytotoxic and anti-migratory candidate for further development as a potential therapeutic agent against cervical cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The interplay of integrin, VE-cadherin, and β-catenin signaling triad in angiogenesis: regulation by Wnt antagonist, secreted frizzled related protein 4 in the tumor angiogenic loop.","authors":"Aishwarya Janaki P, Naisarg Gamit, Preet Agarwal, Arun Dharmarajan, Sudha Warrier","doi":"10.1007/s12032-026-03443-y","DOIUrl":"https://doi.org/10.1007/s12032-026-03443-y","url":null,"abstract":"<p><p>Angiogenesis is the physiological process by which blood vessels form to provide oxygen and nutrients to cells. While angiogenesis can contribute to the therapy of certain ailments, it can also be involved in the pathology of diseases such as cancer. Angiogenesis is performed by endothelial cells (ECs), the innermost layer of blood vessels and the process is dependent on the expression of pro-angiogenic growth factors, cell adhesion proteins, and signaling pathways. Several pathways influence and regulate different stages of blood vessel formation, including EC proliferation, differentiation, migration, polarity, and survival. In tumors, these pathways are dysfunctional, leading to uncontrolled cellular attributes, including deregulated angiogenesis. Specifically, Wnt-β-catenin signaling, a vital cell proliferation pathway, anomalously enhances the expression of pro-angiogenic genes such as vascular endothelial growth factor VEGF, fibronectin and other factors. This review elucidates the role of angiogenic factors and highlights the interplay among VEGF, β-catenin, VE-cadherin, and integrin, all of which are associated with the Wnt-β-catenin pathway. Secreted frizzled related protein 4 (SFRP4) is a well-established Wnt antagonist proven to have anti-tumorigenic, anti-angiogenic, and pro-apoptotic roles. This review proposes a novel role of interaction between SFRP4 and integrin which could disrupt Wnt signaling and inhibit angiogenesis by SFRP4 mediated inhibition of integrin signaling.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes derived from itaconate-treated macrophages promote epithelial-mesenchymal transition, migration, and invasion in MCF-7 breast cancer cells.","authors":"Fatemeh Hosseini Siahi, Azadeh Yektaseresht, Mohammad Reza Tabandeh","doi":"10.1007/s12032-026-03468-3","DOIUrl":"https://doi.org/10.1007/s12032-026-03468-3","url":null,"abstract":"<p><p>Itaconic acid is an immunometabolite that regulates macrophage polarization within the tumor microenvironment and influences tumor progression and invasion. Although its anti-cancer and tumor-promoting effects remain controversial, its role in modulating macrophage-derived exosomes and their impact on breast cancer cells is not well understood. This study investigated the effects of exosomes derived from dimethyl itaconate (DMI)-treated macrophages on epithelial-mesenchymal transition (EMT), apoptosis, migration, and EMT-related miRNAs in MCF7 breast cancer cells. U937 macrophages were treated with 250 µM DMI for 48 h. Exosomes (DMI-EXO) were subsequently isolated, characterized, and used to treat MCF7 cells. The expression of EMT-related proteins (E-cadherin, N-cadherin, ZEB1/2, Slug, and Vimentin) and EMT-associated miRNAs (miR200C-5p, miR30C-5p, miR-638, and miR-137) was evaluated by Western blotting and quantitative real-time PCR, respectively. Apoptosis, cell migration, and invasion were assessed using Annexin V/PI staining, the scratch wound-healing assay, and the Transwell invasion assay, respectively. DMI-EXO treatment significantly increased the expression of the mesenchymal markers N-cadherin, ZEB1/2, Slug, and Vimentin while reducing the epithelial marker E-cadherin. In addition, the expression of EMT-suppressive miRNAs, including miR200C-5p and miR30C-5p, was significantly decreased, whereas no significant change was observed in miR-137 expression following DMI-EXO treatment. DMI-EXO treatment did not significantly alter apoptosis in MCF-7 cells but enhanced cell migration and invasion, as demonstrated by accelerated wound closure in the scratch assay and increased invaded area in the Transwell invasion assay. These findings indicate that DMI-induced macrophage-derived exosomes promote EMT and migration in breast cancer cells by modulating EMT-related proteins and miRNAs. This study provides new evidence that itaconic acid may facilitate breast tumor progression through exosome-mediated communication between macrophages and cancer cells.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}