Cancer gene therapy最新文献_第3页

Potential for enhanced oncolytic HSV-1 therapy via SHED as a vehicle against malignant gliomas. 通过SHED作为恶性胶质瘤载体增强溶瘤性HSV-1治疗的潜力。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2026-08-14 DOI: 10.1038/s41417-026-01072-1

Satoru Kida, Tomoya Oishi, Tomohiro Yamasaki, Yoshinobu Kamio, Tomoya Sakamoto, Toru Kawakatsu, Shinichiro Koizumi, Masahiko Ito, Tetsuro Suzuki, Yoshihiro Otani, Hiroshi Nakashima, Balveen Kaur, Kazuhiko Kurozumi

{"title":"Potential for enhanced oncolytic HSV-1 therapy via SHED as a vehicle against malignant gliomas.","authors":"Satoru Kida, Tomoya Oishi, Tomohiro Yamasaki, Yoshinobu Kamio, Tomoya Sakamoto, Toru Kawakatsu, Shinichiro Koizumi, Masahiko Ito, Tetsuro Suzuki, Yoshihiro Otani, Hiroshi Nakashima, Balveen Kaur, Kazuhiko Kurozumi","doi":"10.1038/s41417-026-01072-1","DOIUrl":"https://doi.org/10.1038/s41417-026-01072-1","url":null,"abstract":"Malignant gliomas are common primary brain tumors. Glioblastoma carries a poor prognosis, with median survival of less than 2 years. Given the urgent need for novel therapies, oncolytic virus (OV) therapy has developed rapidly. However, challenges remain with effective OV delivery to tumor sites and efficient infection of tumor cells. This study investigated the use of stem cells from human exfoliated deciduous teeth (SHED) as a potential vehicle for oncolytic herpes simplex virus-1 therapy (SHED-OV) to enhance treatment efficacy. SHED-OV showed a greater reduction in tumor cell viability in vitro than direct OV infection. Migration assays revealed that SHED-OV actively migrated toward glioma cell-conditioned medium, demonstrating their tumor-homing ability. In vivo experiments demonstrated significantly prolonged survival in both the glioma cell/SHED-OV co-implantation group and the OV-infected glioma cell group compared with controls. In a glioma stem cell model, both SHED-OV and OV alone significantly improved survival compared with controls, with SHED-OV achieving anti-tumor effects comparable to those of direct OV administration and complete tumor regression in a subset of mice. SHED-OV also exhibited tumor-homing ability. These results suggest that SHED could serve as an effective vehicle for OV delivery, potentially improving tumor infection and therapeutic efficacy.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nicotinamide mononucleotide potentiates the anti-tumor efficacy of CAR-NK cell therapy targeting MSLN in ovarian cancer 烟酰胺单核苷酸增强靶向MSLN的CAR-NK细胞治疗卵巢癌的抗肿瘤效果。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2026-08-13 DOI: 10.1038/s41417-026-01071-2

Xin Ouyang, Xiaotong Deng, Qizhao Wang, Minghui Chu, Xinyu Wei, Mengting Wang, Chunming Xiang, Peng Zhang, Zhe Sun, Shijun Shen, Yao Xu

{"title":"Nicotinamide mononucleotide potentiates the anti-tumor efficacy of CAR-NK cell therapy targeting MSLN in ovarian cancer","authors":"Xin Ouyang, Xiaotong Deng, Qizhao Wang, Minghui Chu, Xinyu Wei, Mengting Wang, Chunming Xiang, Peng Zhang, Zhe Sun, Shijun Shen, Yao Xu","doi":"10.1038/s41417-026-01071-2","DOIUrl":"10.1038/s41417-026-01071-2","url":null,"abstract":"Chimeric antigen receptor-engineered NK cells targeting mesothelin (MSLN CAR-NK) have emerged as promising off-the-shelf immunotherapeutics for multiple malignancies. However, their clinical translation remains constrained by inefficient cytotoxic potency and limited persistence. This study investigated the therapeutic potential of nicotinamide mononucleotide (NMN), a metabolic modulator known to enhance immune cell functionality, in augmenting MSLN CAR-NK cell efficacy against ovarian cancer (OC). Through systematic evaluation, we found that NMN supplementation significantly enhanced CAR-NK cell activation marker expression (CD69, NKG2D), degranulation capacity (CD107a+ increased by 21.7 ± 1.1%), and cytokine production (IFN-γ elevated 1.3-fold). In addition, NMN treatment potentiated MSLN CAR-NK cell-mediated cytotoxicity against MSLN+ target cells, achieving 32.8 ± 1.4% specific lysis at an effector-to-target ratio of 25:1, while concurrently reducing cellular apoptosis compared with controls. Mechanistic interrogation via transcriptomic profiling revealed NMN-mediated modulation of PLC-γ phosphorylation cascades and mitochondrial redox homeostasis. Notably, NMN effectively counteracted tumor microenvironment-induced mitochondrial ROS accumulation (reduced by 25.1 ± 0.8% in OC-conditioned medium). Critically, in an OVCAR8-MSLN xenograft model, adoptive transfer of NMN-preconditioned CAR-NK cells led to superior tumor control, reduced proliferation (Ki67), diminished angiogenesis (CD31), and enhanced intratumoral CAR-NK infiltration compared with controls. These findings establish NMN as a clinically relevant adjuvant that augments CAR-NK cell efficacy through dual mechanisms: metabolic enhancement of effector functions and protection against microenvironmental oxidative suppression, thereby offering a translatable strategy to improve CAR-NK therapy for ovarian cancer.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 9","pages":"1081-1091"},"PeriodicalIF":6.4,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Targeting HDAC and proteostasis to eradicate quiescent cancer cells 靶向HDAC和蛋白酶抑制以根除静止癌细胞。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2026-08-13 DOI: 10.1038/s41417-026-01067-y

Qi Jiang, Michelle Ertel, Austin Arrigo, Amjad Hijazzi, Sara Sannino, Jennifer L. Goeckeler-Fried, April Sagan, Ian Beddows, Betsy Ann Varghese, Daniel D. Brown, Wayne Stallaert, Adrian Lee, Amanda M. Clark, Hui Shen, Jeffrey L. Brodsky, Hatice U. Osmanbeyoglu, Ronald J. Buckanovich

{"title":"Targeting HDAC and proteostasis to eradicate quiescent cancer cells","authors":"Qi Jiang, Michelle Ertel, Austin Arrigo, Amjad Hijazzi, Sara Sannino, Jennifer L. Goeckeler-Fried, April Sagan, Ian Beddows, Betsy Ann Varghese, Daniel D. Brown, Wayne Stallaert, Adrian Lee, Amanda M. Clark, Hui Shen, Jeffrey L. Brodsky, Hatice U. Osmanbeyoglu, Ronald J. Buckanovich","doi":"10.1038/s41417-026-01067-y","DOIUrl":"10.1038/s41417-026-01067-y","url":null,"abstract":"Chemotherapy remains the primary treatment for ovarian cancer (OvCa), and chemoresistance drives patient mortality. Cellular quiescence, reversible exit from the cell cycle, increases chemotherapy resistance as chemotherapies primarily target rapidly proliferating cells. Here, we report that CHD4 and MBD3, components of the nucleosome remodeling and deacetylase (NuRD) complex, are downregulated in quiescent OvCa cells (qOvCa). We find that either CHD4 or MBD3 knockdown or histone deacetylase inhibitors (HDACi), induce quiescence in OvCa cells. RNA-Seq and ATAC-seq analysis of HDACi-treated cells confirmed expression changes consistent with induction of quiescence. Additionally, HDACi-treated cells revealed downregulation of the RHO/RAC pathways. Suggesting downregulation of the RAC pathway could play a role in HDACi-mediated quiescence, RAC inhibitors (RACi) similarly induced quiescence. Both HDACi and RACi resulted in nuclear-to-cytoplasmic shifting of the pro-proliferative transcription factor MRTFA. which has been linked to quiescence. Further analysis of HDACi qOvCa indicated multiple alterations in proteostasis, including increased proteasome activity and autophagy. We find qOvCa cells are dependent on these pathways for survival, such that there is profound synergistic OvCa cell death with HDACi and proteasome- or autophagy-inhibitor combination therapy. Combined, this work supports HDACi as pharmacologic means to induce a quiescent state in OvCa cells and sensitize them to proteostasis-targeting drugs.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 9","pages":"1-16"},"PeriodicalIF":6.4,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41417-026-01067-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148764516","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}

引用次数: 0

LncRNA PCAT7 drives tumorigenesis and glycolytic reprogramming in breast cancer via the ceRNA-mediated miR-204-5p/RUNX2 axis LncRNA PCAT7通过cerna介导的miR-204-5p/RUNX2轴驱动乳腺癌的肿瘤发生和糖酵解重编程。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2026-08-10 DOI: 10.1038/s41417-026-01065-0

Pengxiang Zhu, Wei Wu, Yining Han, Zhihan Yao, Rongxuan Xu, Xiaofeng Li

{"title":"LncRNA PCAT7 drives tumorigenesis and glycolytic reprogramming in breast cancer via the ceRNA-mediated miR-204-5p/RUNX2 axis","authors":"Pengxiang Zhu, Wei Wu, Yining Han, Zhihan Yao, Rongxuan Xu, Xiaofeng Li","doi":"10.1038/s41417-026-01065-0","DOIUrl":"10.1038/s41417-026-01065-0","url":null,"abstract":"Breast cancer (BRCA) development is tightly linked to metabolic dysregulation, with enhanced aerobic glycolysis standing out as a key hallmark, and competing endogenous RNA (ceRNA) mechanisms have emerged as critical epigenetic regulators of tumor metabolic pathways—this study thus aimed to explore glycolytic regulation through ceRNA networks in BRCA, with the goal of identifying potential prognostic biomarkers and mechanistic targets. To achieve this, we integrated comprehensive bioinformatics analyses of The Cancer Genome Atlas (TCGA) dataset with experimental validation to identify PCAT7 as a functionally relevant long non-coding RNA (lncRNA), complemented by functional assays including cell proliferation tests, glucose consumption measurements, and lactate production assays, as well as molecular interaction verification using luciferase reporter assays and RNA immunoprecipitation (RIP). Our results showed that PCAT7 is overexpressed in BRCA tissues and correlates with poor patient prognosis; mechanistically, PCAT7 acts as a molecular sponge for miR-204-5p, alleviating its inhibitory effect on RUNX2 and thereby regulating key glycolytic regulators including GLUT1 and PKM2, while silencing PCAT7 suppresses tumor cell proliferation, invasion, migration, and glycolytic activity in vitro. Collectively, this study uncovers a novel ceRNA network involving PCAT7/miR-204-5p/RUNX2 that drives glycolytic metabolism in BRCA, advancing our understanding of epigenetic regulation in cancer metabolism and highlighting PCAT7 as a potential prognostic biomarker for BRCA patients, with future in vivo studies needed to further validate the therapeutic potential of targeting this axis.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 9","pages":"1069-1080"},"PeriodicalIF":6.4,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dynamic expression of CD9 protein in T-cell acute lymphoblastic leukemia. CD9蛋白在t细胞急性淋巴细胞白血病中的动态表达。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2026-08-10 DOI: 10.1038/s41417-026-01066-z

Julie Quessada, Mathis Nozais, Charlotte Savey, Julien Rey, Delphine Potier, Marie Loosveld, Dominique Payet-Bornet

{"title":"Dynamic expression of CD9 protein in T-cell acute lymphoblastic leukemia.","authors":"Julie Quessada, Mathis Nozais, Charlotte Savey, Julien Rey, Delphine Potier, Marie Loosveld, Dominique Payet-Bornet","doi":"10.1038/s41417-026-01066-z","DOIUrl":"https://doi.org/10.1038/s41417-026-01066-z","url":null,"abstract":"T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy affecting both children and adults. Given its persistently poor prognosis, there is a critical need to identify additional factors involved in T-ALL oncogenesis and progression. CD9, a membrane protein of the tetraspanin family implicated in diverse cellular processes, has been associated with prognosis in several cancers, yet its role in T-ALL remains poorly understood. In this study, using a mouse model first, we found that CD9 overexpression is associated with leukemic T cells that have migrated outside the thymus into peripheral tissues. Then, analysis of a human T-ALL cohort shows that CD9 expression is heterogeneous, tends to increase at relapse and is enriched in the TAL1⁺ molecular subtype. We further demonstrate that CD9⁺ cells display enhanced migratory capacity compared with CD9⁻ counterparts, and that CD9 levels affect extracellular vesicle biogenesis. Altogether, our findings support a role for CD9 in T-ALL leukemogenesis and highlight its potential involvement in relapse.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cancer-associated KBTBD4 mutations induce differentiation defects and confer a unique therapeutic vulnerability 癌症相关的KBTBD4突变诱导分化缺陷，并赋予独特的治疗脆弱性。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2026-08-10 DOI: 10.1038/s41417-026-01068-x

Rohit Sivaprasad, Kristijonas Žemaitis, David Linfeldt, Sudip Ghosh, Anne de Snaijer, Mattias Magnusson, Fredrik Ek, Jenny Hansson, Agatheeswaran Subramaniam

{"title":"Cancer-associated KBTBD4 mutations induce differentiation defects and confer a unique therapeutic vulnerability","authors":"Rohit Sivaprasad, Kristijonas Žemaitis, David Linfeldt, Sudip Ghosh, Anne de Snaijer, Mattias Magnusson, Fredrik Ek, Jenny Hansson, Agatheeswaran Subramaniam","doi":"10.1038/s41417-026-01068-x","DOIUrl":"10.1038/s41417-026-01068-x","url":null,"abstract":"Epigenetic regulation governs stem cell fate and perturbations in these mechanisms often lead to tumor development. The CoREST complex, a critical regulator of neural and hematopoietic stem cell differentiation, is recurrently targeted by gain of function mutations in the ubiquitin ligase KBTBD4 in high-risk embryonal brain tumors. However, the tumorigenic potential of these mutations remains unresolved partly due to the challenges in modeling tumors that arise during early brain development. We and others recently demonstrated that small molecule UM171 mimics KBTBD4 mutations by promoting robust CoREST degradation and expansion of hematopoietic stem cells. Leveraging this mechanistic similarity, we modeled KBTBD4 mutations in hematopoietic stem and progenitor cells (HSPCs) and found that mutants induced expansion of immature stem and progenitor populations and impaired lineage differentiation. High-throughput screening identified HDAC inhibitors as specific agents that disrupt mutant KBTBD4 activity, by preventing interaction with the CoREST complex. Using our HSPC model, we demonstrated that the class I HDAC inhibitor mocetinostat alleviated differentiation defects caused by KBTBD4 mutations. Together, these findings reveal the tumorigenic mechanism of KBTBD4 mutations and uncover therapeutic vulnerabilities that may be exploited for clinical applications.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 9","pages":"1092-1098"},"PeriodicalIF":6.4,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41417-026-01068-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705505","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}

引用次数: 0

CLK3 regulates tumor angiogenesis by modulating HIF1α ubiquitination CLK3通过调控HIF1α泛素化调控肿瘤血管生成。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2026-07-27 DOI: 10.1038/s41417-026-01064-1

Jing Shen, Wen Zhang, Zhiqiang Chu, Lei Zhu, Yan Feng, Xuling Sun

{"title":"CLK3 regulates tumor angiogenesis by modulating HIF1α ubiquitination","authors":"Jing Shen, Wen Zhang, Zhiqiang Chu, Lei Zhu, Yan Feng, Xuling Sun","doi":"10.1038/s41417-026-01064-1","DOIUrl":"10.1038/s41417-026-01064-1","url":null,"abstract":"Tumor angiogenesis is a critical driver of cancer progression and is regulated by a complex network of signaling pathways. However, limited therapeutic efficacy and the emergence of drug resistance remain significant obstacles, necessitating the exploration of novel angiogenesis inhibitors, alternative pathways, and reliable biomarkers. In this study, we investigate the role of CDC-like kinase 3 (CLK3) in tumor angiogenesis and its underlying molecular mechanisms. Bioinformatic analysis of clinical datasets revealed that CLK3 expression positively correlated with angiogenesis-related pathways in colorectal cancer. In vitro and in vivo experiments confirmed that CLK3 overexpression promoted tumor angiogenesis, whereas CLK3 knockout inhibited this process. Mechanistically, we demonstrated that CLK3 directly interacted with and stabilizes hypoxia-inducible factor 1-alpha (HIF1α) by inhibiting its ubiquitin-proteasome-mediated degradation. Additionally, CLK3 promoted the phosphorylation of HIF1α at tyrosine residues. Furthermore, our functional assays confirmed that CLK3-mediated tumor angiogenesis was dependent on HIF1α. These findings highlight the importance of CLK3 in regulating tumor angiogenesis, and provide compelling evidence for targeting CLK3 as a potential therapeutic strategy for colorectal cancer treatment.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 9","pages":"1041-1052"},"PeriodicalIF":6.4,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41417-026-01064-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599489","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}

引用次数: 0

HOXC11 promotes head and neck squamous cell carcinomas (HNSCC) progression by regulating SPHK1 through the Wnt signaling pathway HOXC11通过Wnt信号通路调节SPHK1促进头颈部鳞状细胞癌（HNSCC）的进展。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2026-07-25 DOI: 10.1038/s41417-026-01062-3

Jing Zhang, Qionghui Wu, Jingyuan Liu, Shisheng Li

{"title":"HOXC11 promotes head and neck squamous cell carcinomas (HNSCC) progression by regulating SPHK1 through the Wnt signaling pathway","authors":"Jing Zhang, Qionghui Wu, Jingyuan Liu, Shisheng Li","doi":"10.1038/s41417-026-01062-3","DOIUrl":"10.1038/s41417-026-01062-3","url":null,"abstract":"The discovery of potential targets in Head and neck squamous cell carcinomas (HNSCC) through molecular and mechanism analyses is crucial for understanding and treating this disease. This study utilized rigorous methods, including cell lines (FaDu and SCC-15) and a xenograft tumor model. Transfections were conducted using the Lipofectamine 2000 kit, and the evaluation of HOXC11, SPHK1, apoptosis-related protein, and the Wnt signaling pathway was carried out using qPCR and WB methods. The cell proliferation, migration, invasion, and apoptosis were comprehensively evaluated using colony formation, Transwell, wound healing, and flow cytometry, respectively. HOXC11 and SPHK1 are highly expressed in HNSCC and might be involved in the Wnt signaling pathway. HOXC11 promoted cell proliferation, migration, and invasion, inhibiting apoptosis in HNSCC. Silencing SPHK1 inhibited cell progression and dysregulated the Wnt signaling pathway in HNSCC. Overexpressed SPHK1 reversed the functions of sh-HOXC11 in regulating cell progression and the Wnt signaling pathway. HOXC11 promotes HNSCC progression by regulating SPHK1 through the Wnt signaling pathway. Silencing HOXC11 inhibited the tumor growth of HNSCC. Our study demonstrates that HOXC11 promotes HNSCC progression by regulating SPHK1 through the Wnt/β-catenin signaling pathway, identifying a previously unrecognized regulatory axis in HNSCC.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 9","pages":"1029-1040"},"PeriodicalIF":6.4,"publicationDate":"2026-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41417-026-01062-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590512","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}

引用次数: 0

Glypican-3-targeted therapy in hepatocellular carcinoma: biological insights and therapeutic strategies glypican -3靶向治疗肝细胞癌：生物学见解和治疗策略。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2026-07-23 DOI: 10.1038/s41417-026-01058-z

Na Li, Shurong Li, Peng Cao, Mengfan Tang, Junfeng Zhang, Wei Zhang, Jinfeng Liu, Chunping Ye, Dan Wu, Xixi Li, Li Dai, Xianglin Zuo

引用次数: 0

Target therapeutic exploitation of engineered exosome-mediated delivery of ncRNAs in cancer 工程外泌体介导的ncRNAs在癌症中的靶向治疗开发。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2026-07-21 DOI: 10.1038/s41417-026-01059-y

Fatemeh Chaharlang, Nafiseh Mahdipour, Sana Alizadeh Rami, Parichehr Angouti, Alireza Ahmadi, Mohammad Khalaj-Kondori

{"title":"Target therapeutic exploitation of engineered exosome-mediated delivery of ncRNAs in cancer","authors":"Fatemeh Chaharlang, Nafiseh Mahdipour, Sana Alizadeh Rami, Parichehr Angouti, Alireza Ahmadi, Mohammad Khalaj-Kondori","doi":"10.1038/s41417-026-01059-y","DOIUrl":"10.1038/s41417-026-01059-y","url":null,"abstract":"Non-coding RNAs, as microRNAs, long non-coding RNAs, and circular RNAs, are significant modulators of tumor biology and gene expression. miRNAs primarily regulate gene expression at the post-transcriptional level, whereas lncRNAs influence transcriptional activity and epigenetic states. Moreover, circRNAs function as highly stable molecules that shape oncogenic pathways by sequestering miRNAs and interacting with RNA-binding proteins. By addressing these regulatory roles, ncRNAs have emerged as attractive candidates for therapeutic intervention, yet their clinical translation remains limited by rapid degradation, insufficient cellular uptake, and off-target effects. Engineered exosomes—natural nanosized vesicles with strong biocompatibility and barrier-crossing capacity—represent a promising platform to overcome these delivery challenges. This review provides a comprehensive overview of recent advances in exosome engineering for cancer-directed ncRNA delivery. We summarize state-of-the-art strategies designed to enhance loading efficiency, targeting specificity, and therapeutic performance of exosome-mediated delivery systems for miRNAs, lncRNAs, and circRNAs, and outline their growing potential in next-generation cancer therapy.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 6","pages":"758-774"},"PeriodicalIF":6.4,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148547958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0