Oncology Research最新文献

{"title":"The regulatory role of <i>ZFAS1/</i>miRNAs/mRNAs axis in cancer: a systematic review.","authors":"Rahul Kumar Singh, Surojit Mandal, Adrija Mohanta, Ritu Yadav, Rajiv Ranjan Kumar, Rinku Khatkar, Vivek Uttam, Uttam Sharma, Manjit Kaur Rana, Manju Jain, Hardeep Singh Tuli, Aklank Jain","doi":"10.32604/or.2024.050548","DOIUrl":"10.32604/or.2024.050548","url":null,"abstract":"<p><strong>Objectives: </strong>Recently, we and others have demonstrated the involvement of Zinc Finger Antisense 1 (<i>ZFAS1</i>) in cancer development. However, the intricate interplay of <i>ZFAS1</i> with miRNAs and mRNAs remains to be fully understood.</p><p><strong>Materials and methods: </strong>We followed PRISMA guidelines to retrieve and assess the available literature on the topic \"<i>ZFAS1</i>/miRNA/mRNA axis\" and \"Cancer\" from databases such as PubMed, Google Scholar, and ScienceDirect. We also used bioinformatic webtools for analyzing the potential miRNA targets of <i>ZFAS1</i> and its role in survival of cancer patients along with their role in various biological functions and pathways.</p><p><strong>Results: </strong>Our literature search and bioinformatic analysis reveals that <i>ZFAS1</i> serves as a sponge for numerous miRNAs. Among the various targeted miRNAs, miR-150-5p stands out as significantly correlated with <i>ZFAS1</i> across multiple databases (<i>p</i>-value = 3.27e-16, <i>R-</i>value = -0.346). Additionally, our Kaplan-Meier survival analysis indicates a noteworthy association between <i>ZFAS1</i> expression levels and overall poor prognosis and survival rates in ovarian, sarcoma, and pancreatic cancers. We also underscore the involvement of various signaling pathways, including Signal Transducer and Activator of Transcription 3 (STAT3), Spindle and Kinetochore-associated Protein 1 (SKA1), Lysophosphatidic acid receptor 1 (LPAR1), and Wnt β-catenin, in cancer development through the <i>ZFAS1</i>/miRNAs/mRNAs axis. Furthermore, we identify <i>ZFAS1</i>'s pivotal roles in diverse molecular processes, such as RNA binding and ribonucleoprotein formation.</p><p><strong>Conclusion: </strong>In conclusion, this review comprehensively summarizes the latest advancements in understanding the regulatory relationships among <i>ZFAS1</i>, miRNAs, and mRNAs, emphasizing their collective role in cancer development to propose innovative avenues for cancer treatment. We believe that the intricate relationship among the <i>ZFAS1</i>-miRNA-mRNA axis may yield potential therapeutic targets for effective cancer management.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"591-604"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological roles and molecular mechanism of circular RNAs in epithelial-mesenchymal transition of gastrointestinal malignancies.","authors":"Ziyi Fang, Yongfu Shao, Meng Hu, Jianing Yan, Guoliang Ye","doi":"10.32604/or.2024.051589","DOIUrl":"10.32604/or.2024.051589","url":null,"abstract":"<p><p>Circular RNAs (circRNAs) are formed by splicing of precursor RNAs and covalently linked at the 5' and 3' ends. Dysregulated circRNAs are closely related to the epithelial-mesenchymal transition (EMT) of gastrointestinal malignancies. CircRNAs, including circRNA_0008717, circGOT1, circ-DOCK5, circVPS33B, circPVT1, circMET, circ-OXCT1, circ_67835, circRTN4, circ_0087502, circFNDC38, circ_PTEN1, circPGPEP1, and circ-E-Cad are involved in the EMT process of gastrointestinal malignancies through a variety of mechanisms, such as regulating EMT-inducing transcription factors, signaling pathways, and tumor microenvironments. Gastrointestinal (GI) malignancies are common malignant tumors worldwide, and the heterogeneity and easy metastasis of gastrointestinal malignancies limit the effectiveness of medical treatments. Therefore, investigating the molecular mechanisms involved in the pathogenesis of gastrointestinal malignancies is essential for clinical treatment. This article summarizes the biological roles and molecular mechanism of circRNAs in EMT of gastrointestinal malignancies, providing a theoretical basis for applying EMT-related circRNAs in targeted therapy.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"549-566"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarkers for predicting bladder cancer therapy response.","authors":"Ioana Maria Mihai, Gang Wang","doi":"10.32604/or.2024.055155","DOIUrl":"10.32604/or.2024.055155","url":null,"abstract":"<p><p>The advent of precision medicine has underscored the importance of biomarkers in predicting therapy response for bladder cancer, a malignancy marked by considerable heterogeneity. This review critically examines the current landscape of biomarkers to forecast treatment outcomes in bladder cancer patients. We explore a range of biomarkers, including genetic, epigenetic, proteomic, and transcriptomic indicators, from multiple sample sources, including urine, tumor tissue and blood, assessing their efficacy in predicting responses to chemotherapy, immunotherapy, and targeted therapies. Despite promising developments, the translation of these biomarkers into clinical practice faces significant challenges, such as variability in biomarker performance, the necessity for large-scale validation studies, and the integration of biomarker testing into routine clinical workflows. We also highlight the need for standardized methodologies and robust assays to ensure consistency and reliability. Future directions point towards longitudinal studies and the development of combination biomarker panels to enhance predictive accuracy. This review emphasizes the transformative potential of predictive biomarkers in improving patient outcomes and advocates for continued collaborative efforts to overcome existing barriers in this rapidly evolving field.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"533-547"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astragalus polysaccharide enhances the therapeutic efficacy of cisplatin in triple-negative breast cancer through multiple mechanisms.","authors":"L I Sun, Shichao Zhuo, Xiaoxin Li, Husheng Kong, Weiwei DU, Chong Zhou, Junxing Huang","doi":"10.32604/or.2024.050057","DOIUrl":"10.32604/or.2024.050057","url":null,"abstract":"<p><strong>Background: </strong>Cisplatin (DDP) has been used in the treatment of various human cancers. However, DDP alone lacks efficacy in treating triple-negative breast cancer (TNBC), and its clinical application is often hampered by side effects. <i>Astragalus polysaccharide</i> (APS) is one of the active components extracted from <i>Astragalus membranaceus</i> and has gained attention for its various biological properties. This research is aimed to evaluate the effectiveness of a combination of APS and DDP on TNBC and explore the potential mechanisms.</p><p><strong>Methods: </strong>The efficacy and mechanisms of single or combined treatment were evaluated using Cell Counting Kit-8 (CCK8) assay, Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining, wound healing assay, trans-well invasion/migration assay, hematoxylin-eosin (HE) staining, immunohistochemical (IHC) staining, Western Blot (WB) analysis, and fluorescence-activated cell sorting (FACS). An orthotopic model of TNBC was used to assess the <i>in vivo</i> treatment efficacy of single or combination treatment.</p><p><strong>Results: </strong>APS significantly enhanced the anti-proliferative, anti-migratory, and anti-invasive effects of DDP on TNBC cells. The combination of APS and DDP downregulated anti-apoptotic genes (Bcl2 and Bcl-xL) while upregulating pro-apoptotic genes (Puma, Cle-Caspase3, Cle-PARP), leading to enhanced apoptosis. This combination treatment increased E-cadherin levels, decreased Vimentin, Snail, Slug, and Twist levels, and effectively suppressed epithelial-mesenchymal transition (EMT)-associated cell invasion. In the orthotopic model of TNBC, a synergistic reduction in tumor growth was observed in mice treated with APS and DDP. Additionally, the combination of APS and DDP induced the infiltration of CD8⁺ T lymphocytes into the tumor immune microenvironment.</p><p><strong>Conclusion: </strong>The combination of APS and DDP exhibits more potent tumor inhibition and anti-tumor immunity than either agent alone, representing a novel approach to enhance therapeutic efficacy without increasing the side effects of DDP.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"641-651"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preventive effects of low-dose radiation and hypofractionated radiation plus anti-programmed cell death protein 1 on lung metastasis in breast cancer.","authors":"Shuang Chen, Xuemei Deng, Xingting He, Kewei Xiang, Guihong Chen, Hongru Yang","doi":"10.32604/or.2024.052133","DOIUrl":"10.32604/or.2024.052133","url":null,"abstract":"<p><strong>Background: </strong>Previous experiments have demonstrated that hypofractionated radiation therapy (HFRT), low-dose radiation therapy (LDRT), and combined anti-programmed cell death protein 1 (αPD-1) can enhance the abscopal effect. Combined with the phenomenon of low prognosis in patients with breast cancer lung metastasis, our study establishes a mouse model and changes the irradiation regimen of LDRT to explore its preventive effect on breast cancer lung metastasis.</p><p><strong>Methods: </strong>The breast cancer subcutaneous graft tumor model was developed. Two-lung prophylactic LDRT was performed prior to the onset of lung metastases, in combination with HFRT (8 Gy, 3f), and αPD-1 (200 μg, 4f) therapy. We watched and documented the tumor volume, survival duration, and number of lung metastases. Furthermore, after labeling the corresponding cells using markers, we detected immune-related cell infiltration by immunohistochemistry and flow cytometry, such as T cells. We also determined the expression of cytokines (IFN-γ and TNF-α) by enzyme-linked immunosorbent assay.</p><p><strong>Result: </strong>The triple therapy (HFRT+LDRT+αPD-1) resulted in tumor shrinkage and prolonged survival in mice, with median survival extending from 35 to 52 days. The most notable decrease in the quantity of advanced lung metastatic nodules in breast cancer was observed with the triple therapy (HFRT+LDRT+αPD-1) (<i>p</i> < 0.05). Furthermore, according to immunohistochemistry and flow cytometry, the triple treatment (HFRT+LDRT+αPD-1) showed the greatest expression of CD8⁺ T cells. Additionally, the ratio of CD8⁺/CD4⁺ T cells was considerably greater than that of the groups (<i>p</i> < 0.0001). Triple therapy (HFRT+LDRT+αPD-1) increased the recruitment of DCs cells, promoted IFN-γ and TNF-α expression, and curbed the aggregation of MDSCs cells (<i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>Prophylactic LDRT to the lungs, based on HFRT and αPD-1, can enhance anti-tumor efficacy and prevent advanced lung metastases from breast cancer. The process involves boosting the recruitment of DCs and CD8⁺ T cells, preventing MDSC cell aggregation, and lessening the tumor microenvironment's immunosuppressive effects.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"687-694"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ultrasound genomics related mitochondrial gene signature for prognosis and neoadjuvant chemotherapy resistance in triple negative breast cancer.","authors":"Huafang Huang, Guilin Wang, Dongyun Zeng, Luz Angela Torres-DE LA Roche, Rui Zhuo, Rudy Leon DE Wilde, Wanwan Wang, Ulf D Kahlert, Wenjie Shi","doi":"10.32604/or.2024.054642","DOIUrl":"10.32604/or.2024.054642","url":null,"abstract":"<p><strong>Background: </strong>Neoadjuvant chemotherapy (NAC) significantly enhances clinical outcomes in patients with triple-negative breast cancer (TNBC); however, chemoresistance frequently results in treatment failure. Consequently, understanding the mechanisms underlying resistance and accurately predicting this phenomenon are crucial for improving treatment efficacy.</p><p><strong>Methods: </strong>Ultrasound images from 62 patients, taken before and after neoadjuvant therapy, were collected. Mitochondrial-related genes were extracted from a public database. Ultrasound features associated with NAC resistance were identified and correlated with significant mitochondrial-related genes. Subsequently, a prognostic model was developed and evaluated using the GSE58812 dataset. We also assessed this model alongside clinical factors and its ability to predict immunotherapy response.</p><p><strong>Results: </strong>A total of 32 significant differentially expressed genes in TNBC across three groups indicated a strong correlation with ultrasound features. Univariate and multivariate Cox regression analyses identified six genes as independent risk factors for TNBC prognosis. Based on these six mitochondrial-related genes, we constructed a TNBC prognostic model. The model's risk scores indicated that high-risk patients generally have a poorer prognosis compared to low-risk patients, with the model demonstrating high predictive performance (<i>p</i> = 0.002, AUC = 0.745). This conclusion was further supported in the test set (<i>p</i> = 0.026, AUC = 0.718). Additionally, we found that high-risk patients exhibited more advanced tumor characteristics, while low-risk patients were more sensitive to common chemotherapy drugs and immunotherapy. The signature-related genes also predicted immunotherapy response with a high accuracy of 0.765.</p><p><strong>Conclusion: </strong>We identified resistance-related features from ultrasound images and integrated them with genomic data, enabling effective risk stratification of patients and prediction of the efficacy of neoadjuvant chemotherapy and immunotherapy in patients with TNBC.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"631-640"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: MYBL2 is targeted by miR-143-3p and regulates breast cancer cell proliferation and apoptosis.","authors":"","doi":"10.32604/or.2024.056911","DOIUrl":"https://doi.org/10.32604/or.2024.056911","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504017X15135941182107.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"739"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915048/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Terpinen-4-ol suppresses proliferation and motility of cutaneous squamous cell carcinoma cells by enhancing calpain-2 expression.","authors":"Dongyun Rong, Yushen Su, Zhirui Zeng, Yan Yang, Honguan Lu, Y U Cao","doi":"10.32604/or.2024.050661","DOIUrl":"10.32604/or.2024.050661","url":null,"abstract":"<p><strong>Background: </strong>Terpinen-4-ol (T4O), a key constituent of tea tree essential oil and various aromatic plants, has shown promising antiproliferative and pro-apoptotic effects in melanoma and other cancer types. However, its efficacy against cutaneous squamous cell carcinoma (cSCC) remains unclear. Thus, in this study, we investigated the <i>in vivo</i> and <i>in vitro</i> effects of T4O on cSCC cell lines and preliminarily explored its impacting pathways.</p><p><strong>Methods: </strong>Using CCK8 and assay colony formation, we assessed the viability of cSCC A431, SCL-1, and COLO-16 cells treated with T40 at varying concentrations (0, 1, 2, and 4 μM). Flow cytometry was employed to evaluate T4O's effect on cSCC cell's cycle progression and apoptosis induction. Additionally, western blotting was utilized to examine the expression intensities of N-cadherin and E-cadherin, two indicative markers of the epithelial-mesenchymal transition (EMT) pathway. T4O's <i>in vivo</i> effect on inhibiting tumor progression was evaluated on an established xenograft tumor model. Then, the molecular mechanisms of T4O's antitumor effect were explored by an integrated genome-wide transcriptomics and proteomics study on cSCC A431c cells. Finally, calpain-2's potential mediator role in T4O's anti-tumor mechanism was investigated in calpain-2 knockdown cell lines prepared via siRNA transfection.</p><p><strong>Result: </strong>It's demonstrated that T4O treatment inhibited cSCC proliferation, clonogenicity, migration, and invasion while inducing apoptosis and suppressing the EMT pathway. T4O administration also inhibited cSCC tumorigenesis in the xenograft tumor model. RNA-sequencing and iTRAQ analysis detected significant upregulation of calpain-2 expression in T4O-treated cSCC cells. Western blotting confirmed that T4O significantly increased calpain-2 expression and promoted proteolytic cleavage of β-catenin and caspase-12, two calpain-2 target proteins. Importantly, siRNA-mediated calpain-2 knockdown relieved T4O's suppressive effect on cSCC cell proliferation and motility. Mechanistically, T4O upregulates calpain-2 expression and promotes the cleavage of β-catenin and caspase-12, with siRNA-mediated calpain-2 knockdown mitigating T4O's suppressive effects.</p><p><strong>Conclusion: </strong>These findings suggest that T4O's antitumor activity in cSCC is mediated through the upregulation of calpain-2 expression and subsequent modulation of β-catenin and caspase-12.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"605-616"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915078/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dibenzo [a, c] phenazin-11-yl(phenyl) methanone (SBLJ23), a novel selective inhibitor targeting JAK2^V617F mutation in myeloproliferative neoplasms.","authors":"Mohammad Abohassan, Mesfer Mohammad Al Shahrani, Sarah Khaled Alouda, Prasanna Rajagopalan","doi":"10.32604/or.2024.056256","DOIUrl":"10.32604/or.2024.056256","url":null,"abstract":"<p><strong>Background: </strong>The JAK2^V617F mutation plays a crucial part in the pathogenesis of myeloproliferative neoplasms (MPN), which includes polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) leading to aberrant proliferation and survival of hematopoietic cells. Alongside the challenges of drug resistance and side effects, identifying novel compounds that selectively target JAK2^V617F could provide more effective and safer therapeutic options for patients with MPNs.</p><p><strong>Materials and methods: </strong>We employed computational approaches like high-throughput virtual screening, molecular dynamics simulations (MDS), and binding free energy calculations to identify inhibitors targeting wild and mutant JAK2 kinases. JAK2^V617F positive HEL, wild type JAK2 positive TF-1, and non-cancerous Vero cells were used for <i>in vitro</i> validations.</p><p><strong>Results: </strong>SBLJ23 emerged as a top candidate inhibitor with specificity for JAK2^V617F. Protein-ligand interaction studies and MDS revealed stable interactions and binding of SBLJ23 over the simulation period, with Root Mean Square Deviation (RMSD) indicating consistent binding after 1t15ns. SBLJ23 displayed a half maximal inhibitory concentration (IC₅₀) value of 522.4 nM against the JAK2 enzyme. The compound exhibited inhibition of cell proliferation in HEL and TF-1 cells, with half maximal cell growth inhibitory concentration (GI₅₀) values of 2.51 and 15.87 µM, respectively. Moreover, SBLJ23 induced G₂/M cell cycle arrest in HEL cells to facilitate apoptosis in these cell lines. The compound significantly reduced the percentage of phospho JAK2 and phospho STAT3 in HEL cells.</p><p><strong>Conclusion: </strong>High binding affinity, stable interaction profile, favorable binding free energy, and <i>in vitro</i> validations claim SBLJ23 as a potential lead compound against JAK2^V617F and suggest further development and optimization towards clinical application in managing myeloproliferative neoplasms.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"675-685"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Magnetic melamine cross-linked polystyrene-alt-malic anhydride copolymer: Synthesis, characterization, paclitaxel delivery, cytotoxic effects on human ovarian and breast cancer cells.","authors":"Razieh Momen-Mesgin, Jafar Rezaie, Vahid Nejati, Peyman Najafi Moghadam","doi":"10.32604/or.2024.054487","DOIUrl":"10.32604/or.2024.054487","url":null,"abstract":"<p><strong>Objectives: </strong>Due to systematic side effects, there is a growing interest in nanoparticle formulation of anticancer drugs. Here, we aimed to synthesize poly (styrene-alt-maleic anhydride) cross-linked by melamine (PSMA/Me) and coated with magnetite nanoparticles (MNPs) PSMA/Me/Fe₃O₄. In addition, we aimed to load paclitaxel (PTX) into PSMA/Me/Fe₃O₄ for drug delivery and anticancer investigations.</p><p><strong>Methods: </strong>Novel PSMA/Me was synthesized via free radical copolymerization, coated with Fe₃O₄, and then used as a transporter for PTX delivery. Fabricated copolymer was characterized using SEM, TGA, and XRD techniques. Drug release rate and loading efficiency were investigated. Human ovarian cancer cells (Skov-3) and breast cancer cells (MCF-7 cells) were incubated with the serial concentration of either free PTX or PSMA/Me/Fe₃O₄/PTX for cell viability and IC₅₀ analysis for 24 and 48 h.</p><p><strong>Results: </strong>Characterization methods confirmed PSMA/Me copolymer formation. The results showed a significant encapsulation efficiency of 83%. The drug release analysis exhibited that PSMA/Me/Fe₃O₄/PTX may be considered pH-sensitive nanocarriers. PSMA/Me/Fe₃O₄/PTX reduced cell viability both dose and time-dependently (<i>p</i> < 0.05). IC₅₀ values of PSMA/Me/Fe₃O₄/PTX were low when compared to free PTX either 24 or 48 h post-treatment.</p><p><strong>Conclusions: </strong>Our results indicated that PSMA/Me/Fe₃O₄/PTX was more cytotoxic than PTX in both cancer cells. Findings indicated the potential of PSMA/Me/Fe₃O₄/PTX as an anticancer nanocarrier system.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"665-674"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915072/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}