Medical Oncology最新文献

{"title":"Effect of pyrogallol nanocomposite on miRNA and its associated pathways during radiation-induced toxicity in small intestine of irradiated Balb/C mice.","authors":"Sreemadhi Parvathikandhan, Sivaa Varshini Anbarasu, Krithika Narayanan, Rubin Nishanth Armstrong, Vadivel Vellingiri, Devipriya Nagarajan, Rekha Arcot, Musab Hamed Saeed, Muthu Thiruvengadam, Naiyf S Alharbi","doi":"10.1007/s12032-025-02989-7","DOIUrl":"10.1007/s12032-025-02989-7","url":null,"abstract":"<p><p>Cancer is the abnormal and uncontrolled growth of cells that changes the structure of nearby cells or tissues. Cancer treatment strategies include surgery, chemotherapy, immunotherapy, and radiotherapy. Radiation therapy is one of the most frequently used cancer treatment modalities. Ionizing radiation not only kills cancer cells but also affects surrounding normal cells, causing extensive damage to all organs including the liver, kidneys, and intestines. Thus, identifying radioprotective agents is crucial to reduce the side effects of radiotherapy. Recently, nanocomposites have played a crucial role in cancer diagnosis and treatment as well as in reducing radiation-induced side effects. In this study, we tested pyrogallol nanocomposites for radiation-induced toxicity. Pyrogallol is a catechin molecule found in oak, eucalyptus, and other hardwood plants and is an amino polysaccharide produced by the deacetylation of chitin found in crustaceans and insects. In this study, pyrogallol and chitosan nanoparticles were blended to form a pyrogallol nanocomposite (PyNC). We investigated changes in miRNA expression in the small intestine of irradiated BALB/c mice. BALB/c mice were divided into four groups: control, irradiated (10 Gy), irradiated (10 Gy) + PyNC (40 μg/kg body weight), and PyNC alone (40 μg/kg body weight). We analyzed miRNA expression, apoptotic genes, inflammatory genes, and fibrotic genes using real-time PCR, and apoptotic proteins were analyzed by Western blotting and immunohistochemistry. Our results revealed that radiation modulated miRNA expression patterns regulated by PyNC. Analysis of the miRNA online database revealed that the miRNA targets were casp9, IL7, IL7R, JUN, MMP9, Bcl2, and SMAD4. Furthermore, real-time PCR, Western blotting, and immunohistochemistry analyses revealed that radiation increased apoptotic proteins, inflammatory markers, and TGF-β and its associated molecules, which effectively decreased upon PyNC treatment in irradiated BALB/c mice. Additionally, PyNC treatment inhibited DNA fragmentation and oxidative stress in the small intestine of irradiated BALB/c mice. Overall, we suggest that PyNC effectively protects the small intestine from radiation-induced toxicity by altering miRNAs and their associated molecular targets, including apoptosis, inflammation, and fibrosis. However, overexpression or knockout studies of miRNAs during radiation-induced toxicity are warranted.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 10","pages":"457"},"PeriodicalIF":3.5,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960308","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":"Machine learning integration of bulk and single-cell RNA-seq data reveals glycolytic heterogeneity in colorectal cancer.","authors":"Yuanyuan Du, Zefeng Miao, Peng Li, Dan Feng, Mulin Liu, Aifang Ji, Shijun Li","doi":"10.1007/s12032-025-03007-6","DOIUrl":"10.1007/s12032-025-03007-6","url":null,"abstract":"<p><p>As one of the most prevalent malignancies worldwide, colorectal cancer (CRC) exhibits a strong metabolic dependency on glycolysis, which fuels tumor expansion and shapes an immunosuppressive microenvironment. Despite its clinical significance, the regulatory landscape and cellular diversity of glycolytic metabolism in CRC require systematic exploration. Multi-omics datasets (bulk/scRNA-seq and spatial transcriptomics) were analyzed to quantify glycolytic signatures. Core regulatory genes were selected via integrated pathway mapping and a machine learning framework incorporating five-feature selection algorithms. Cellular subpopulations were delineated by metabolic profiles, with niche interactions modeled through ligand-receptor network analysis. Findings were validated across multicenter cohorts. Our analyses identified a tumor subpopulation characterized by a High Glycolytic State (HGS), displaying elevated glycolytic signature alongside stem-like properties. Spatial profiling demonstrated relative enrichment of HGS cells in central tumor regions, potentially reflecting adaptation to nutrient-limited conditions. Among the molecular features associated with HGS maintenance, five candidate regulators (PFKP, ERO1A, FKBP4, HDLBP, HSPA5) showed correlation with unfavorable clinical outcomes. Our study characterizes the metabolic heterogeneity of CRC and suggests a potential role for HGS cells in shaping the tumor microenvironment. The molecular features identified here may offer insights into metabolic dependencies that could be explored for future therapeutic targeting.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 10","pages":"458"},"PeriodicalIF":3.5,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960390","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":"Wedelolactone induces pyroptosis to suppress retinoblastoma by inhibiting the Nrf2/Keap1 signaling pathway.","authors":"Yizhou Jiang, Hua Jiang, Guitao Wu, Ningdong Pang, Chuanqiang Niu, Zhouping Wang, Haibo Li","doi":"10.1007/s12032-025-02916-w","DOIUrl":"10.1007/s12032-025-02916-w","url":null,"abstract":"<p><strong>Background: </strong>Retinoblastoma is an intraocular malignancy with limited therapeutic options, imposing a severe health burden on young patients. Wedelolactone (WDL), a natural product from E. prostrata, possesses an anti-retinoblastoma activity, with the underlying regulatory mechanism remaining unknown.</p><p><strong>Methods: </strong>Retinoblastoma cell lines and xenograft nude mouse models were treated with WDL and RTA-408, an agonist for nuclear factor-erythroid 2-related factor 2 (Nrf2). Western blotting was conducted to determine the protein expression levels of kelch-like ECH-associated protein 1 (Keap1) and Nrf2. We performed the cell counting kit-8 assay, the 5-ethynyl-2-deoxyuridine staining, and flow cytometry to detect cell viability, proliferation, and apoptosis, respectively. The tumor progression in vivo was evaluated via the measurement of volume, weight, and proliferation levels of solid tumors. Monosodium urate crystal was applied to activate pyroptosis which was assessed by the expression detection of pyroptosis-related indicators.</p><p><strong>Results: </strong>WDL treatment elevated the expression of Keap1 and reduced the level of Nrf2. RTA-408 suppressed WDL-induced pyroptosis of retinoblastoma cells and reversed the effect of WDL on inhibiting retinoblastoma cell proliferation, promoting tumor cell apoptosis, and repressing the growth of solid tumors of the xenograft models. In addition, monosodium urate-induced pyroptosis partially restored the anti-retinoblastoma effect of WDL impaired by RTA-408.</p><p><strong>Conclusion: </strong>WDL triggers pyroptosis by inhibiting the Nrf2/Keap1 signaling pathway to exert anti-retinoblastoma effects.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 10","pages":"456"},"PeriodicalIF":3.5,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12397164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960501","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":"miRNA-mediated resistance mechanisms in prostate cancer: implications for targeted therapy and metastatic progression.","authors":"Mostafa M Mostafa, Mostafa K Abd El-Aziz, Doha El-Sayed Ellakwa","doi":"10.1007/s12032-025-03006-7","DOIUrl":"10.1007/s12032-025-03006-7","url":null,"abstract":"<p><p>Prostate cancer (PCa) remains a leading cause of cancer-related morbidity and mortality in men, with progression to castration-resistant and metastatic disease driven largely by therapeutic resistance. While numerous reviews have cataloged dysregulated microRNAs (miRNAs) in prostate cancer, this review offers a novel, mechanism-centered synthesis focused specifically on miRNA-mediated resistance pathways across standard treatment modalities-including androgen deprivation therapy (ADT), enzalutamide, docetaxel, and radiotherapy. Rather than providing a broad survey of miRNA functions, we prioritize miRNAs with robust experimental validation in PCa (e.g., miR-21, miR-34a, miR-205, miR-141) and analyze their roles in convergent resistance mechanisms such as PI3K/AKT activation, EMT, DNA repair, and AR variant signaling. We critically evaluate the functional evidence linking these miRNAs to treatment failure, highlighting how their dysregulation promotes survival, stemness, and adaptive responses within the tumor microenvironment-particularly through extracellular vesicle (EV)-mediated communication and hypoxia-driven signaling. Although circulating miRNA signatures show promise as non-invasive biomarkers, we explicitly acknowledge major translational challenges, including poor reproducibility across cohorts, lack of standardized normalization methods, tumor heterogeneity, and inefficient in vivo delivery of miRNA-based therapeutics. This review distinguishes between well-supported preclinical findings and the current absence of clinically validated miRNA applications, emphasizing that miRNA mimics and antagomiRs remain investigational. We conclude that future progress depends on rigorous validation in prospective trials, improved delivery platforms (e.g., EV-based systems), and integration of miRNA profiles with clinical and genomic data. By focusing on resistance mechanisms rather than general dysregulation, this work provides a conceptual framework for prioritizing miRNAs with the highest potential for impacting precision oncology in prostate cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 10","pages":"454"},"PeriodicalIF":3.5,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960316","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 diverse roles of circular RNAs in cholangiocarcinoma.","authors":"Yanhui Zhang, Xue Xing, Jia Liu, Li Hou, Yi Xu, Bo Zhai, Haonan Feng, Changwen Guo, Gang Tan, Daolin Ji","doi":"10.1007/s12032-025-03018-3","DOIUrl":"10.1007/s12032-025-03018-3","url":null,"abstract":"<p><p>Cholangiocarcinoma (CCA) is a malignant tumor that develops in the extrahepatic bile duct, that is, from the left and right hepatic ducts to the lower end of the common bile duct. Because of its indeterminate etiology, difficulties in the diagnosis of early lesions, easy invasion and metastasis and resistance to chemotherapeutic drugs, the trend of mortality rate deterioration of patients with CCA has not been fundamentally reversed. And the molecular mechanisms underlying the development of CCA are not well characterized. Circular RNA (CircRNA) is an endogenous non-coding RNA with a circular structure. Recent studies have found circRNA involved in multiple physiological processes and participated in the proliferation, invasion, metastasis, immunomodulation, angiogenesis, biometabolism, and chemoresistance of many malignancies, including CCA, pancreatic cancer, liver cancer, and gastric cancer. In this review, we summarize what has been published so far to be related to the biogenesis, functions, and characteristics of circRNAs in CCA and the potential clinical prospects.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 10","pages":"455"},"PeriodicalIF":3.5,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960466","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":"Magnetic hyperthermia-based therapies for cancer targeting: current progress and future perspectives.","authors":"Prinsy Rana, Garima, Sushma Devi, Gurpreet Kaur, Sachin Kumar Singh, Neeraj Mittal","doi":"10.1007/s12032-025-03020-9","DOIUrl":"10.1007/s12032-025-03020-9","url":null,"abstract":"<p><p>Cancer has complicated pathological events, and conventional cancer therapy has limitations in the lack of selectivity, cytotoxicity, and the development of multidrug resistance. Hyperthermia, based on mild elevation in temperature up to 45 °C, can result in cancer cell death. However, the clinical applicability of MNPs for heating malignant cells is impeded by the difficulties of efficiently and selectively heating the tumors. The intravenous delivery of cancer-targeted magnetic nanoparticles (MNPs), combined with the application of an external magnetic field, is designed to elevate the temperature in tumor tissue where the nanoparticles (NPs) are concentrated. While preclinical developments in magnetic hyperthermia (MHT) are promising, several challenges must be addressed before this method can be applied in clinical settings. This review article will explore the role of hyperthermia in inducing tumor cell death, the principles of utilizing MHT for cancer targeting, the potential advantages of combination therapies, the biocompatibility of MNPs, and the specific challenges associated with implementing MHT as a treatment for cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 10","pages":"453"},"PeriodicalIF":3.5,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960326","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":"Progress in the mechanistic understanding of NETs formation in cancer.","authors":"Chuanhong Luo, Xie Xiong, Chen Fang, Biao Yu, Xiaoying Qian, Weiwei Hong, Song Hong, Hui Li, Yong Wang, Yong Li","doi":"10.1007/s12032-025-03010-x","DOIUrl":"10.1007/s12032-025-03010-x","url":null,"abstract":"<p><p>Recent studies have revealed that the tumor microenvironment (TME) mediates neutrophil activation through multicomponent collaborative regulatory mechanisms, serving as a key driver of NETs formation. Cytokines, platelets, and complements activate neutrophil signaling pathways, ultimately forming NETs with protumorigenic properties in the TME. Notably, exogenous stimuli such as surgery, chronic stress, and pathogens can regulate NETs formation by remodeling the TME. However, the regulatory factors that induce NETs formation have not yet been systematically elucidated. Despite the identification of several factors that initiate the formation of NETs, the potential involvement of additional mechanisms remains inadequately understood. There is an urgent need for thorough mechanistic investigations utilizing cell lines and animal models in cancer. These studies will yield essential insights necessary for the formulation of targeted therapeutic approaches. This review delves into the mechanisms behind neutrophil extracellular traps (NETs) formation, tumor microenvironmental regulation of NETs formation, and exogenous stimuli that mediate tumor biological behaviors by inducing NETs. Gaining insight into these mechanisms will enhance our understanding of NETs and aid in crafting more precise strategies to inhibit tumor progression.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 10","pages":"451"},"PeriodicalIF":3.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960395","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 role of phosphatidylcholine metabolism in tumors.","authors":"Lulu Li, Yongxiu Huang, Yaoqi Gui, Wenqiong Xiang, Min Yang, Yu Hou, Meixi Peng","doi":"10.1007/s12032-025-03017-4","DOIUrl":"10.1007/s12032-025-03017-4","url":null,"abstract":"<p><p>Phosphatidylcholine (PC), a core component of eukaryotic cell membranes essential for maintaining membrane integrity, has emerged as a critical regulator in oncogenic metabolic reprogramming. Accumulating evidence reveals that dysregulated PC metabolism constitutes a central mechanism driving malignant tumor progression. This review systematically delineates the biosynthetic pathways (Kennedy pathway, PEMT pathway, Lands cycle) and catabolic processes (phospholipase-mediated hydrolysis via PLA₂, PC-PLC, and PLD) governing PC homeostasis. We highlight how PC metabolic networks orchestrate pro-tumorigenic effects via multifaceted mechanisms, such as enhancing membrane biosynthesis to support rapid tumor proliferation, activating some proliferative signaling cascades coupled with apoptosis suppression, remodeling the immunosuppressive microenvironment, et al. Notably, small-molecule inhibitors targeting key PC metabolic enzymes (e.g., RSM-932A, FIPI) demonstrate promising anti-tumor efficacy in preclinical models, though therapeutic outcomes are constrained by metabolic plasticity and tumor heterogeneity. By integrating recent advances in lipidomics and spatial metabolomics, this synthesis not only deciphers the evolutionary logic underlying PC-driven oncogenesis but also proposes innovative therapeutic strategies combining metabolic inhibitors with immune checkpoint modulators. Our analysis provides a conceptual framework for targeting phospholipid vulnerabilities in cancer, paving the way for precision oncology applications.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 10","pages":"450"},"PeriodicalIF":3.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960429","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":"Advances in cancer therapy using fluorinated chitosan: a promising nanoplatform for drug delivery.","authors":"Devesh U Kapoor, Anil Pareek, Saraswati Patel, Mohammad Fareed, Omar Awad Alsaidan, Bhupendra G Prajapati","doi":"10.1007/s12032-025-03022-7","DOIUrl":"10.1007/s12032-025-03022-7","url":null,"abstract":"<p><p>Chitosan, a naturally derived polysaccharide, has gained considerable attention as a biomaterial for drug delivery due to its excellent biocompatibility, biodegradability, and mucoadhesive properties. However, its limited solubility and compatibility with hydrophobic drugs restrict broader applications. Recent advances in the chemical modification of chitosan specifically through fluorination have significantly improved its performance in nanomedicine. Fluorinated chitosan (FCS) exhibits enhanced hydrophobicity, chemical and thermal stability, and improved drug encapsulation efficiency, making it highly effective for cancer therapy. This review comprehensively examines the synthesis techniques of FCS nanoparticles, such as grafting, ionic gelation, and microemulsion, and evaluates how these influence particle size, stability, and drug loading. The multifunctional role of FCS in targeted cancer drug delivery, photodynamic therapy, immunotherapy, and gene editing is critically analyzed, supported by in vitro and in vivo studies demonstrating improved tumor accumulation, cellular uptake, and immune modulation. Despite its promise, FCS presents challenges such as toxicity concerns and regulatory complexities, which must be addressed for clinical translation. Future prospects include developing stimuli-responsive systems and expanding FCS applications beyond oncology. Overall, FCS represents a transformative platform in nanotechnology, offering new avenues for precision drug delivery and personalized cancer treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 10","pages":"452"},"PeriodicalIF":3.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960320","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":"A novel long non-coding RNA, PICSAR, promotes thyroid cancer progression through the hsa-miR-320A/hsa-miR-485/RAPGEFL1 axis.","authors":"Maryam Hejazi, Tahmineh Jafari, AmirHossein Yari, Ramin Heshmat, Bagher Larijani, Samaneh Ahvaz, Omid Pourbagherian, Seyed Mohammad Tavangar, Gita Shafiee, Amir Ali Mokhtarzadeh","doi":"10.1007/s12032-025-02987-9","DOIUrl":"10.1007/s12032-025-02987-9","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Among endocrine cancers, thyroid carcinoma (TC) is the most prevalent and ranks sixth in global mortality rates. Aberrant expression of long non-coding RNA (lncRNAs) is associated with the progression of various human cancers, including TC. The role of PICSAR lncRNA (LINC00162) has been validated in different human cancers. Therefore, this study aimed to assess the expression levels and functions of lncRNA PICSAR in thyroid cancer tumorigenesis. This comprehensive approach combined in silico and in vitro methods to explore the molecular mechanisms and clinical significance of PICSAR in thyroid cancer. This work assessed the expression of the long non-coding RNA LINC00162 and identified differentially expressed genes (DEGs) using the Cancer Genome Atlas (TCGA) database. Interactions among LINC00162, hsa-miR-320A, hsa-miR-485, and RAPGEFL1 were investigated using the LncACT and miRDB databases. Bioinformatics techniques were employed to conduct functional enrichment analysis to clarify the relevant molecular pathways. For the investigation of LINC00162 expression in TC samples, 50 matched samples of thyroid carcinoma and adjacent normal tissue were gathered. Real time PCR was used to objectively evaluate the expression levels of the targeted genes. Every tissue sample was examined pathologically. A specific siRNA was transfected into a thyroid cancer cell line to examine the functional role of LINC00162. The impact of LINC00162 silencing was then assessed by measuring the level of target genes expression following the transfection. Based on TCGA-THCA analysis and qRT-PCR on tissue samples, LINC00162 (PICSAR) was markedly overexpressed in thyroid cancer tissues compared to normal samples. However, no discernible correlation was found between LINC00162 expression and the pathological characteristics of thyroid cancer. Our bioinformatics predictions based on lncRNA-microRNA interactions demonstrate that LINC00162 acts as a molecular sponge for the downregulated microRNAs hsa-miR-320A and hsa-miR-485 in thyroid cancer. RAPGEFL1, a gene associated with the development of thyroid cancer, is upregulated in conjunction with this downregulation. The LINC00162-miRNA-RAPGEFL1 axis is involved in critical carcinogenic processes, including thiamine metabolism, cell cycle control, and folate biosynthesis, according to functional enrichment analysis. Additionally, a bioinformatics study revealed a negative association between PICSAR and the NUDT3 gene, while a positive correlation was found with the SNX18P14 gene. Thyroid cancer cells transfected with LINC00162-specific siRNA showed significant downregulation of LINC00162 and RAPGEFL1, alongside an increase in hsa-miR-320A and hsa-miR-485, ultimately inhibiting the growth of thyroid cancer. These findings suggest that targeting PICSAR may offer a treatment strategy for thyroid cancer by altering important biological processes. In conclusion, LINC00162, which is overexpressed in thyroid cancer, acts as a mol","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 10","pages":"448"},"PeriodicalIF":3.5,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960396","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}