American journal of cancer research最新文献

{"title":"STOML2 inhibits sorafenib-induced ferroptosis in hepatocellular carcinoma via p-AKT signaling pathway.","authors":"Ruiqi Yin, Yifeng Tao, Jiahao Han, Jubo Zhang, Kangkang Yu, Yahui Zheng, Xiaoqi Li, Chong Huang","doi":"10.62347/SUTJ3506","DOIUrl":"https://doi.org/10.62347/SUTJ3506","url":null,"abstract":"<p><p>Tyrosine kinase inhibitor resistance is a key factor affecting the prognosis of patients with advanced hepatocellular carcinoma (HCC). Previously, our group demonstrated that HCC patients with high stomatin-like protein 2 (STOML2) expression were poorly sensitive to systemic therapy. Whether STOML2 is involved in sorafenib resistance is unclear. Recent mechanistic studies have demonstrated that selective activation of ferroptosis pathways is expected to restore sorafenib sensitivity. The aim of the present study was to investigate the STOML2-ferroptosis axis and its contribution to sorafenib resistance. In this study, STOML2 expression was detected in tissue microarrays from patients with primary HCC and in human cell lines. Functional proliferative clone formation assay was used to study the biological function of STOML2. Ferroptosis was detected by flow cytometry, cellular lipid peroxidation and the malondialdehyde (MDA) test. Western blotting and qPCR assays were used to verify the STOML2-AKT-solute carrier family 7 membrane 11 (SLC7A11) axis and to explore the possible mechanism of the combination of LY294002 (an AKT inhibitor) in patients with advanced HCC. The results indicated that patients with poor efficacy demonstrated higher expression of STOML2 compared with that in samples derived from patients with good efficacy. Knockdown of STOML2 expression inhibited colony formation and IC₅₀ in HCC cell lines treated with sorafenib. High STOML2 expression was negatively correlated with ferroptosis as shown by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis. STOML2 inhibited ferroptosis by activating the AKT-SLC7A11 axis, which promoted increased intracellular antioxidant capacity. The AKT inhibitor LY294002 exhibited synergistic antitumor effects with sorafenib in HCC. In conclusion, the present study demonstrated that STOML2 could enhance the AKT-SLC7A11-mediated antioxidant capacity in HCC, inhibit ferroptosis and reduce the sensitivity of HCC to sorafenib, providing a theoretical basis for the combination of LY294002 and sorafenib.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1614-1628"},"PeriodicalIF":3.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between immune checkpoint inhibitors and cardiovascular risks: a nationwide self-controlled case series study.","authors":"Wei-Ting Chang, Hui-Wen Lin, Chin-Hsiu Liu, Sheng-Hsiang Lin, Yi-Heng Li","doi":"10.62347/ZUUA2691","DOIUrl":"https://doi.org/10.62347/ZUUA2691","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) are widely used for cancer treatment but are linked to potential cardiotoxicity. The time-dependent effects of ICIs on cardiovascular outcomes remain unclear. This study explores associations between ICI use and cardiovascular events. This self-controlled case series (SCCS) analyzed cancer patients who received ICIs from January 2019 to December 2020 using the National Health Insurance Research Database (NHIRD). Exposure periods were defined as the duration of ICI prescriptions plus 90 days. Poisson regression estimated incidence rate ratios (IRRs) for heart failure (primary outcome) and arterial events or perimyocarditis (secondary outcomes) during and after ICI exposure compared to baseline. Among 1,146 ICI users, 15 developed heart failure, 33 experienced arterial events, and 11 had perimyocarditis. Cardiovascular events were uncommon but showed elevated risks for heart failure (IRR: 7.73; CI: 2.05-29.14, P<0.01) and perimyocarditis (IRR: 8.25; CI: 1.60-42.50, P = 0.01) within 30 days of ICI exposure. Subgroup analysis identified higher risks in patients aged ≥65, males, and those with diabetes, hypertension, or hyperlipidemia. Furthermore, when focusing on patients who received more than two doses of ICIs or exclusively anti-PD-1 inhibitors, we observed a similarly increased risk of HF within 30 days post-exposure. Collectively, ICI exposure significantly elevates the risk of heart failure and perimyocarditis within 30 days, particularly in older adults and those with preexisting cardiovascular risk factors.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1820-1828"},"PeriodicalIF":3.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_0000190 inhibits the progression of triple negative breast cancer by regulating miR-301a/MEOX2 pathway.","authors":"Heng Liu, Xiunan Li, Gangyue Wang, Yu Ren, Zhenlie Fan, Xin Tang","doi":"10.62347/AMTI5713","DOIUrl":"https://doi.org/10.62347/AMTI5713","url":null,"abstract":"<p><p>Circular RNA (circRNA) and microRNA (miRNA) play critical roles in regulating proliferation, apoptosis, and invasion in triple-negative breast cancer (TNBC) cells. To investigate their functional significance, we employed quantitative real-time PCR (qRT-PCR) to assess the differential expression of circ_0000190, miR-301a, and mesenchyme homeobox 2 (MEOX2) between TNBC cell lines and normal breast epithelial cells. Subsequently, we established overexpression and knockdown systems for these molecules to examine their effects on TNBC cell proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT). Additionally, we evaluated the impact of circ_0000190 overexpression on tumor growth using a mouse xenograft model, measuring tumor volume and weight. Our findings revealed that circ_0000190 and MEOX2 expression were significantly downregulated (P<0.05) in TNBC cells compared to normal breast epithelial cells, whereas miR-301a was upregulated (P<0.05). Knockdown of circ_0000190 promoted TNBC cell proliferation, migration, invasion, and EMT, while suppressing apoptosis. Mechanistically, circ_0000190 functioned as a molecular sponge for miR-301a, and its overexpression significantly inhibited miR-301a expression (P<0.001). Notably, miR-301a mimics partially reversed the suppressive effects of circ_0000190 overexpression on proliferation, migration, invasion, and EMT, as well as its pro-apoptotic effects (P<0.001). Furthermore, we identified MEOX2 as a direct target of miR-301a. MEOX2 knockdown attenuated the inhibitory effects of miR-301a silencing on proliferation, migration, invasion, and EMT, while also counteracting its pro-apoptotic function. In vivo experiments demonstrated that circ_0000190 overexpression significantly reduced tumor volume and weight (P<0.001), concomitant with elevated MEOX2 mRNA and protein levels (P<0.001) and decreased miR-301a expression (P<0.001). In conclusion, our study elucidates that circ_0000190 suppresses TNBC progression by downregulating miR-301a and upregulating MEOX2, forming a competitive endogenous RNA (ceRNA) network of circRNA-miRNA-mRNA.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1559-1577"},"PeriodicalIF":3.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070081/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictive role of peripheral blood indicators in the prognosis of patients with cutaneous squamous cell carcinoma treated with immune checkpoint inhibitors.","authors":"Xiaoyue Xiao, Qianying Yu, Bingying Han, Min Fu, Mingling Chen","doi":"10.62347/KZOQ9722","DOIUrl":"https://doi.org/10.62347/KZOQ9722","url":null,"abstract":"<p><p>This study aimed to explore the predictive role of peripheral blood indicators in the prognosis of cutaneous squamous cell carcinoma (cSCC) patients treated with immune checkpoint inhibitors (ICIs). Clinical data of 139 cSCC patients receiving ICIs treatment were retrospectively collected. Peripheral blood indicators, including blood cell counts, neutrophil-to-lymphocyte ratio (NLR), liver and kidney function markers, and inflammation markers, were examined. A binary logistic regression model was used to identify risk factors for non-response to ICIs, and a predictive model was constructed. Additionally, multiple linear regression and Pearson correlation analysis were employed to assess relevant influences and relationships. Results showed that immunotherapy timing, lymphocyte count, NLR, and C-reactive protein (CRP) were influencing factors for non-response to ICIs (all P<0.05). The area under the curve (AUC) for these indicators in predicting non-response risk was 0.651 (95% CI: 0.529-0.773), 0.671 (95% CI: 0.542-0.801), 0.775 (95% CI: 0.682-0.868), and 0.717 (95% CI: 0.573-0.861), respectively. The combined AUC of these four factors was 0.878 (95% CI: 0.790-0.966), with sensitivity and specificity of 76.0% and 93.0%, respectively. After internal verification, the constructed model exhibited predicted sensitivity and specificity of 80.00% and 94.29% respectively. Multiple linear regression analysis indicated that these four factors were independent predictors of progression-free survival (PFS) in cSCC patients. Immunotherapy timing, NLR, and CRP were negatively correlated with PFS (r = -0.235, -0.330, -0.494), while lymphocyte count was positively correlated with PFS (r = 0.326). In conclusion, peripheral blood indicators are valuable for predicting the response to ICIs in cSCC and can influence patients' PFS.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1705-1718"},"PeriodicalIF":3.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Small protein DDX11-AS1-ORF encoded by lncRNA DDX11-AS1 promotes colorectal cancer progression through VEGFA-activated p38-MAPK pathway.","authors":"Yuanfang Cheng, Jiajie Dong, Kai Shang, Lejing Zhang, Yongwei Chen, Rihui Li, Zhaoxi Li, Zheying Zhang, Yajuan Wang","doi":"10.62347/VRJE7714","DOIUrl":"https://doi.org/10.62347/VRJE7714","url":null,"abstract":"<p><p>This study aims to investigate the expression, function, and mechanism of action of the small protein DDX11 antisense RNA 1 - open reading frame (DDX11-AS1-ORF), encoded by the long non-coding RNA (lncRNA) DDX11 antisense RNA 1 (DDX11-AS1), in the progression of colorectal cancer (CRC). The expression levels of DDX11-AS1 were assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis in 10 pairs of colorectal cancer tissues and corresponding non-tumor tissues. Functional evaluations of DDX11-AS1 and DDX11-AS1-ORF were conducted using cell counting kit-8 (CCK8) assays, colony formation assays, Transwell migration assays, and in vitro tube formation assays. The coding potential of DDX11-AS1 was validated by western blot and immunofluorescence. The activation of the p38 mitogen-activated protein kinase (p38-MAPK) pathway by DDX11-AS1-ORF through VEGFA was analyzed using western blot. The results showed that DDX11-AS1 was significantly upregulated in colorectal cancer tissues and cells, promoting cancer cell proliferation, migration, and angiogenesis. DDX11-AS1 translated into a functional small protein, DDX11-AS1-ORF, which independently enhanced the malignant behaviors of tumor cells. DDX11-AS1-ORF promoted colorectal cancer progression by activating the p38-MAPK signaling pathway through Vascular Endothelial Growth Factor A (VEGFA). The critical role of the p38-MAPK pathway in DDX11-AS1-ORF mediated tumor promotion was confirmed using the p38-MAPK pathway inhibitor SB203580. In conclusion, the small protein DDX11-AS1-ORF, encoded by DDX11-AS1, plays a crucial role in the development of colorectal cancer by promoting tumor proliferation, migration, and angiogenesis through the activation of VEGFA and the p38-MAPK signaling pathway. These findings provide a novel potential target for molecular targeted therapy in colorectal cancer.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1662-1672"},"PeriodicalIF":3.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA XIST enhances gastric cancer cell function by regulating STAT3/PD-L1 axis as a competing endogenous RNA for miR-124.","authors":"Gaowa Sharen, Haoyu Meng, Lei Zhang, Kejian Liu, Yu Wang, Defang Zhao","doi":"10.62347/JBHH9597","DOIUrl":"https://doi.org/10.62347/JBHH9597","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the role and underlying mechanisms of the long non-coding RNA (lncRNA) X inactive-specific transcript (XIST) in gastric cancer (GC).</p><p><strong>Methods: </strong>Real-time quantitative PCR (RT-qPCR), CCK-8, colony formation, flow cytometry, Transwell, and scratch assays were used to evaluate the biological effects of XIST and miR-124 in GC cells. Bioinformatics analysis and dual-luciferase reporter (DLR) assays identified interactions between XIST, miR-124, and STAT3. Western blotting and RT-qPCR assessed changes in downstream targets, while a xenograft tumor model evaluated the in vivo effects of XIST knockdown.</p><p><strong>Results: </strong>XIST was significantly upregulated, and miR-124 was downregulated in GC tissues and cell lines, with the strongest effects observed in MGC803 cells. Knockdown of XIST or overexpression of miR-124 suppressed GC cell proliferation, colony formation, migration, invasion, and promoted apoptosis, effects that were reversed by miR-124 inhibitors. Bioinformatics and DLR assays confirmed that XIST directly targeted miR-124 and regulated STAT3 expression. XIST knockdown increased miR-124 levels, reducing STAT3, PD-1, PD-L1, N-cadherin, and MMP9 expression, while elevating E-cadherin levels; these effects were reversed by miR-124 inhibitors. Additionally, sh-STAT3 mitigated the pro-tumorigenic effects of pcDNA-XIST, confirming the regulatory relationship. In vivo, XIST knockdown suppressed tumor growth by increasing miR-124 expression.</p><p><strong>Conclusion: </strong>XIST promotes STAT3 expression by competitively binding to miR-124, thereby promoting GC progression. Targeting the XIST/miR-124/STAT3 axis may represent a potential therapeutic strategy for GC.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1597-1613"},"PeriodicalIF":3.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070116/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role and mechanisms of m6A demethylases in digestive system tumors.","authors":"Lingli Jiang, Yang Chen, Qing Luo, Guanbin Song","doi":"10.62347/XMAF1290","DOIUrl":"https://doi.org/10.62347/XMAF1290","url":null,"abstract":"<p><p>Digestive system tumors are common malignancies in humans, often accompanied by high mortality and poor prognosis. Therefore, intensive research on the pathogenesis of digestive system tumors is imperative. N6-methyladenosine (m6A) is the most common RNA modification in eukaryotes and exerts regulatory effects on RNA expression and metabolism, including splicing, translation, stability, decay, and transport. m6A demethylases belong to the AlkB family of dioxygenases that can catalyze m6A demethylation. Accumulating evidence in recent years has shown that abnormal m6A levels caused by m6A demethylases play crucial roles in different aspects of human cancer development. In this review, we comprehensively summarize the recent findings on the functions and underlying molecular mechanisms of m6A demethylases in cell proliferation, apoptosis, migration, invasion, metastasis, angiogenesis, resistance to chemo- and radiotherapy, and the tumor immune microenvironment (TIME) of digestive system tumors. Furthermore, we discuss the therapeutic potential of targeting these m6A demethylases for treatment.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1436-1460"},"PeriodicalIF":3.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploiting replication stress for synthetic lethality in MYC-driven cancers.","authors":"Yuan Zhang, Meng Ye, Xin Luan, Zhe Sun, Wei-Dong Zhang","doi":"10.62347/RTVX8866","DOIUrl":"https://doi.org/10.62347/RTVX8866","url":null,"abstract":"<p><p>The oncoprotein MYC, overexpressed in more than 70% of human cancers, plays a pivotal role in regulating gene transcription and has long been recognized as a promising target for cancer therapy. However, no MYC-targeted drug has been approved for clinical use, largely due to the lack of a well-defined druggable domain and its nuclear localization. MYC-overexpressing cancer cells exhibit increased replication stress, driven by factors such as elevated replication origin firing, nucleotide depletion, replication-transcription conflicts, and heightened reactive oxygen species (ROS) production. Simultaneously, MYC activates compensatory mechanisms, including enhanced DNA repair, checkpoint-mediated cell cycle regulation, and metabolic reprogramming, to mitigate this stress and support cell survival. Interfering with these compensatory pathways exacerbates replication stress, leading to synthetic lethality in MYC-driven cancer cells. In this review, we summarize recent advances in leveraging replication stress to achieve synthetic lethality in MYC-driven cancers. Furthermore, we discuss current strategies targeting replication stress, highlighting new opportunities for the development of therapies against MYC-driven malignancies.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 4","pages":"1461-1479"},"PeriodicalIF":3.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nomogram model based on tumor-infiltrating lymphocytes and clinical characteristics to predict prognosis of patients with laryngeal squamous cell carcinoma.","authors":"Xiaojuan Zhou, Jiaqi Tan, Xueying Wang, Xin Zhang, Susheng Miao, Yong Liu, Junrong Wang, Guolin Tan","doi":"10.62347/MKFI3976","DOIUrl":"https://doi.org/10.62347/MKFI3976","url":null,"abstract":"<p><p>Head and neck carcinomas are the sixth most common cancers worldwide, with laryngeal squamous cell carcinoma (LSCC) being the second most prevalent subtype. Improving survival outcomes in LSCC patients remains a critical clinical challenge. This retrospective study aimed to develop a nomogram model integrating tumor-infiltrating lymphocytes (TILs) and clinicopathological characteristics to predict the prognosis of LSCC patients. The nomogram model was constructed using Cox and Lasso regression analyses and was subsequently evaluated through receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA). Data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were utilized for model validation and to further elucidate the role of TILs and immune responses in LSCC. This study cohort included LSCC patients diagnosed by pathological examination between 2011 and 2014 at Xiangya Hospital and Harbin Medical University Cancer Hospital. A total of 412 patients were assigned to the training cohort and 140 patients to the test cohort for validation. The final nomogram model integrated TNM stage, TILs, PLR, BMI, age, differentiation and NLR. The area under the curve (AUC) was 0.745, indicating strong calibration and clinical utility. Kaplan-Meier survival curves demonstrated significant discrimination. TILs were positively correlated with immune cell abundance and the expression of immune-related genes. In conclusion, the nomogram model based on TILs and clinicopathological features effectively predicts the prognosis of LSCC patients.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 3","pages":"976-990"},"PeriodicalIF":3.6,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11982727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multifunctional nanoplatforms based on RNA interference for glioma treatment.","authors":"Ting Zhao, Hongping Ju, Zihao Chen","doi":"10.62347/AERM5603","DOIUrl":"https://doi.org/10.62347/AERM5603","url":null,"abstract":"<p><p>Glioma is the most common malignant tumor in the central nervous system. Currently, common clinical treatments for glioma include surgery, radiation therapy, chemotherapy and immunotherapy, among which the combination of chemotherapy and immunotherapy has attracted wide attention. However, the ability of chemotherapeutic agents and immune checkpoint blockers to reach gliomas is limited due to the existence of blood brain/tumor barrier (BBB/BTB). RNA interference (RNAi) technology enables specific silencing of target genes associated with cancer therapy, so it has been used as an emerging potential cancer treatment strategy. However, Small interference RNA (siRNA) is easily degraded by serum endonuclease, which can be quickly filtered and cleared by the glomerulus. Therefore, design and construction of safe and effective delivery systems is conducive to improving the stability of siRNA and the efficiency of gene silencing. This review focuses on the research progress of nano delivery system based on RNA interference for glioma treatment.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 3","pages":"835-854"},"PeriodicalIF":3.6,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11982710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}