Cancer gene therapy最新文献_第3页

Role of non-coding RNA in lineage plasticity of prostate cancer. 非编码 RNA 在前列腺癌血统可塑性中的作用

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-04 DOI: 10.1038/s41417-024-00834-z

Wenhui Tan, Changkai Xiao, Min Ma, Youhan Cao, Zhenguo Huang, Xiaolan Wang, Ran Kang, Zhenfa Li, Ermao Li

{"title":"Role of non-coding RNA in lineage plasticity of prostate cancer.","authors":"Wenhui Tan, Changkai Xiao, Min Ma, Youhan Cao, Zhenguo Huang, Xiaolan Wang, Ran Kang, Zhenfa Li, Ermao Li","doi":"10.1038/s41417-024-00834-z","DOIUrl":"10.1038/s41417-024-00834-z","url":null,"abstract":"<p><p>The treatment of prostate cancer (PCa) has made great progress in recent years, but treatment resistance always develops and can even lead to fatal disease. Exploring the mechanism of drug resistance is of great significance for improving treatment outcomes and developing biomarkers with predictive value. It is increasingly recognized that mechanism of drug resistance in advanced PCa is related to lineage plasticity and tissue differentiation. Specifically, one of the mechanisms by which castration-resistant prostate cancer (CRPC) cells acquire drug resistance and transform into neuroendocrine prostate cancer (NEPC) cells is lineage plasticity. NEPC is a subtype of PCa that is highly aggressive and lethal, with a median survival of only 7 months. With the development of high-throughput RNA sequencing technology, more and more non-coding RNAs have been identified, which play important roles in different diseases through different mechanisms. Several ncRNAs have shown great potential in PCa lineage plasticity and as biomarkers. In the review, the role of ncRNA in PCa lineage plasticity and its use as biomarkers were reviewed.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142575078","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

BAIAP2L2 promotes the malignancy of hepatocellular carcinoma via GABPB1-mediated reactive oxygen species imbalance BAIAP2L2 通过 GABPB1 介导的活性氧失衡促进肝细胞癌的恶性发展。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-04 DOI: 10.1038/s41417-024-00841-0

Wenbo Jia, Bin Xu, Liang Yu, Yanzhi Feng, Jinyi Wang, Chao Xu, Litao Liang, Yongping Zhou, Wenzhou Ding, Lianbao Kong

{"title":"BAIAP2L2 promotes the malignancy of hepatocellular carcinoma via GABPB1-mediated reactive oxygen species imbalance","authors":"Wenbo Jia, Bin Xu, Liang Yu, Yanzhi Feng, Jinyi Wang, Chao Xu, Litao Liang, Yongping Zhou, Wenzhou Ding, Lianbao Kong","doi":"10.1038/s41417-024-00841-0","DOIUrl":"10.1038/s41417-024-00841-0","url":null,"abstract":"Hepatocellular carcinoma (HCC) is a common type of cancer worldwide and ranks as the fourth leading cause of cancer-related deaths. This research investigation identified an upregulation of BAI1-associated protein 2-like 2 (BAIAP2L2) in HCC tissues, which was found to be an independent prognostic factor for overall survival in HCC patients. BAIAP2L2 was observed to enhance cell proliferation, metastasis, stemness, cell cycle progression, and inhibit apoptosis in HCC. Mechanistically, NFκB1 was found to stimulate BAIAP2L2 transcription by directly binding to its promoter region. BAIAP2L2 interacts with GABPB1 to inhibit its ubiquitin-mediated degradation and promote its nuclear translocation. BAIAP2L2 inhibits the levels of reactive oxygen species (ROS) by regulating GABPB1, thereby promoting cancer properties in HCC and reducing the sensitivity of HCC to lenvatinib. In summary, this study elucidates the role and underlying mechanism of BAIAP2L2 in HCC, providing a potential biomarker and therapeutic target for this disease.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 12","pages":"1868-1883"},"PeriodicalIF":4.8,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41417-024-00841-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142575070","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

Baicalein inhibits cell proliferation and induces apoptosis in brain glioma cells by downregulating the LGR4-EGFR pathway 黄芩素通过下调 LGR4-EGFR 通路抑制脑胶质瘤细胞增殖并诱导其凋亡。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-10-28 DOI: 10.1038/s41417-024-00825-0

Xiaobing Zhang, Xian Shao, Qingquan Bao, Lingyan He, Xuchen Qi

{"title":"Baicalein inhibits cell proliferation and induces apoptosis in brain glioma cells by downregulating the LGR4-EGFR pathway","authors":"Xiaobing Zhang, Xian Shao, Qingquan Bao, Lingyan He, Xuchen Qi","doi":"10.1038/s41417-024-00825-0","DOIUrl":"10.1038/s41417-024-00825-0","url":null,"abstract":"Patients diagnosed with brain glioma have a poor prognosis and limited therapeutic options. LGR4 is overexpressed in brain glioma and involved in the tumorigenesis of many tumors. Baicalein (BAI) is a kind of flavonoid that has exhibited anti-tumor effects in various tumors. Nevertheless, the functions and associations of BAI and LGR4 in brain glioma remain unclear. In this study, Gene Expression Profiling Interactive Analysis and Human Protein Atlas databases were used to perform expression and survival analysis of LGR4 in brain glioma patients. Subsequently, the significance of LGR4-EGFR in brain glioma cells (HS683 and KNS89) and brain glioma animal models was explored by RNA interference and subcutaneous transplantation. Additionally, brain glioma cells were treated with BAI to explore the roles and mechanisms of BAI in brain glioma. The results showed that LGR4 was highly expressed in brain glioma and was related to a poor prognosis. LGR4 knockdown repressed the proliferation and EGFR phosphorylation but induced apoptosis in brain glioma cells. However, these effects were reversed by EGFR overexpression and CBL knockdown. In contrast, both in vitro and in vivo experiments revealed that LGR4 overexpression facilitated brain glioma cell malignant behavior and promoted tumor development, but these effects were rescued by BAI and an EGFR inhibitor. Furthermore, si-LGR4 accelerated EGFR protein degradation, while oe-LGR4 exhibited the opposite effect. Without affecting normal cellular viability, BAI inhibited malignant behavior, interacted with LGR4, and blocked the LGR4-EGFR pathway for brain glioma cells. In conclusion, our data suggested that BAI inhibited brain glioma cell proliferation and induced apoptosis by downregulating the LGR4-EGFR pathway, which provides a novel strategy and potential therapeutic targets to treat brain glioma.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 12","pages":"1856-1867"},"PeriodicalIF":4.8,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41417-024-00825-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521094","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

SEMA7A-mediated juxtacrine stimulation of IGFBP-3 upregulates IL-17RB at pancreatic cancer invasive front SEMA7A介导的IGFBP-3并体刺激可上调胰腺癌浸润前沿的IL-17RB。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-10-24 DOI: 10.1038/s41417-024-00849-6

Yi-Ing Chen, Sui-Chih Tien, Yi-Ling Ko, Chin-Chun Chang, Min-Fen Hsu, Hung Jen Chien, Hsuan-Yu Peng, Yung-Ming Jeng, Yun-Wen Tien, Yu-Ting Chang, Ming-Chu Chang, Chun-Mei Hu

{"title":"SEMA7A-mediated juxtacrine stimulation of IGFBP-3 upregulates IL-17RB at pancreatic cancer invasive front","authors":"Yi-Ing Chen, Sui-Chih Tien, Yi-Ling Ko, Chin-Chun Chang, Min-Fen Hsu, Hung Jen Chien, Hsuan-Yu Peng, Yung-Ming Jeng, Yun-Wen Tien, Yu-Ting Chang, Ming-Chu Chang, Chun-Mei Hu","doi":"10.1038/s41417-024-00849-6","DOIUrl":"10.1038/s41417-024-00849-6","url":null,"abstract":"Tumor invasion is the hallmark of tumor malignancy. The invasive infiltration pattern of tumor cells located at the leading edge is highly correlated with metastasis and unfavorable patient outcomes. However, the regulatory mechanisms governing tumor malignancy at the invasive margin remain unclear. The IL-17B/IL-17RB pathway is known to promote pancreatic cancer invasion and metastasis, yet the specific mechanisms underlying IL-17RB upregulation during invasion are poorly understood. In this study, we unveiled a multistep process for IL-17RB upregulation at the invasive margin, which occurs through direct communication between tumor cells and fibroblasts. Tumor ATP1A1 facilitates plasma membrane expression of SEMA7A, which binds to and induces IGFBP-3 secretion from fibroblasts. The resulting gradient of IGFBP-3 influences the direction and enhances IL-17RB expression to regulate SNAI2 in invasion. These findings highlight the importance of local tumor-fibroblast interactions in promoting cancer cell invasiveness, potentially leading to the development of new therapeutic strategies targeting this communication.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 12","pages":"1840-1855"},"PeriodicalIF":4.8,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41417-024-00849-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495725","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

Correction: Arsenic trioxide and p97 inhibitor synergize against acute myeloid leukemia by targeting nascent polypeptides and activating the ZAKα–JNK pathway 更正：三氧化二砷和 p97 抑制剂通过靶向新生多肽和激活 ZAKα-JNK 通路对急性髓性白血病有协同作用。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-10-21 DOI: 10.1038/s41417-024-00848-7

Shufeng Xie, Hui Liu, Shouhai Zhu, Zhihong Chen, Ruiheng Wang, Wenjie Zhang, Huajian Xian, Rufang Xiang, Xiaoli Xia, Yong Sun, Jinlan Long, Yuanli Wang, Minghui Wang, Yixin Wang, Yaoyifu Yu, Zixuan Huang, Chaoqun Lu, Zhenshu Xu, Han Liu

引用次数: 0

γ-Glutamylcyclotransferase is transcriptionally regulated by c-Jun and controls proliferation of glioblastoma stem cells through Notch1 levels γ-谷氨酰环基转移酶受c-Jun转录调控，并通过Notch1水平控制胶质母细胞瘤干细胞的增殖。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-10-11 DOI: 10.1038/s41417-024-00835-y

Kozue Nose, Keiko Taniguchi, Mitsugu Fujita, Chiami Moyama, Masaya Mori, Mizuki Ishita, Tatsushi Yoshida, Hiromi Ii, Toshiyuki Sakai, Susumu Nakata

{"title":"γ-Glutamylcyclotransferase is transcriptionally regulated by c-Jun and controls proliferation of glioblastoma stem cells through Notch1 levels","authors":"Kozue Nose, Keiko Taniguchi, Mitsugu Fujita, Chiami Moyama, Masaya Mori, Mizuki Ishita, Tatsushi Yoshida, Hiromi Ii, Toshiyuki Sakai, Susumu Nakata","doi":"10.1038/s41417-024-00835-y","DOIUrl":"10.1038/s41417-024-00835-y","url":null,"abstract":"Glioblastoma stem cells (GSCs) have been reported to cause poor prognosis of glioblastoma by contributing to therapy resistance. γ-Glutamylcyclotransferase (GGCT) is highly expressed in various cancer types, including glioblastoma, and its inhibition suppresses cancer cell growth. However, the mechanism of GGCT overexpression and its function in GSCs are unknown. In this study, we show that GGCT is highly expressed in GSCs established from a mouse glioblastoma model and its knockdown suppresses their proliferation. Effects of NRas and its downstream transcription factor c-Jun on GGCT expression were analyzed; NRas knockdown reduced c-Jun and GGCT expression. Knockdown of c-Jun also reduced expression levels of GGCT and inhibited cell proliferation. Consistent with this, pharmacological inhibition of c-Jun with SP600125 reduced GGCT and inhibited GSC proliferation. Furthermore, the GGCT promoter-reporter assay with mutagenesis demonstrated that c-Jun regulates the activity of the GGCT promoter via AP-1 consensus sequence. Gene expression analysis revealed that GGCT knockdown showed a repressive effect on the Delta-Notch pathway and decreased Notch1 expression. Notch1 knockdown alone inhibited the GSC proliferation, confirming that Notch1 is functional in this model. Forced expression of the Notch1 intracellular domain restored the growth inhibitory effect of GGCT knockdown. Moreover, GGCT knockdown inhibited GSC tumorigenic potential in vivo. These results indicate that GGCT, whose expression is promoted by c-Jun, plays an important role in the proliferation and tumorigenic potential of GSCs, and that the phenotype caused by its knockdown is contributed by a decrease in Notch1. Thus, GGCT may represent a novel therapeutic target for attacking GSCs.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 12","pages":"1-9"},"PeriodicalIF":4.8,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41417-024-00835-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142406162","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

Intraperitoneal administration of adeno-associated virus encoding microRNA-29b for the treatment of peritoneal metastasis 腹膜内注射编码 microRNA-29b 的腺相关病毒治疗腹膜转移瘤。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-10-10 DOI: 10.1038/s41417-024-00837-w

Yuki Kaneko, Hideyuki Ohzawa, Yuki Kimura, Rei Takahashi, Misaki Matsumiya, Kohei Tamura, Yurie Futoh, Hideyo Miyato, Shin Saito, Hironori Yamaguchi, Yoshinori Hosoya, Ryota Watano, Hiroaki Mizukami, Naohiro Sata, Joji Kitayama

{"title":"Intraperitoneal administration of adeno-associated virus encoding microRNA-29b for the treatment of peritoneal metastasis","authors":"Yuki Kaneko, Hideyuki Ohzawa, Yuki Kimura, Rei Takahashi, Misaki Matsumiya, Kohei Tamura, Yurie Futoh, Hideyo Miyato, Shin Saito, Hironori Yamaguchi, Yoshinori Hosoya, Ryota Watano, Hiroaki Mizukami, Naohiro Sata, Joji Kitayama","doi":"10.1038/s41417-024-00837-w","DOIUrl":"10.1038/s41417-024-00837-w","url":null,"abstract":"This study explores a novel therapeutic approach for peritoneal metastasis (PM) using AAV-mediated delivery of tumor suppressor microRNA-29b (miR-29b) to peritoneal mesothelial cells (PMC). AAV serotypes 2 and DJ demonstrate high transduction efficiency for human and murine PMC, respectively. In vitro analysis indicates that AAV vectors encoding miR-29b precursor successfully elevate miR-29b expression in PMC and their secreted small extracellular vesicle (sEV), thereby inhibiting mesothelial mesenchymal transition and reducing subsequent attachment of tumor cells. A single intraperitoneal (IP) administration of AAV-DJ-miR-29b demonstrates robust and sustained transgene expression, suppressing peritoneal fibrosis and inhibiting the development of PM from gastric and pancreatic cancers. Additionally, AAV-DJ-miR-29b enhances the efficacy of IP chemotherapy using paclitaxel, restraining the growth of established PM. While conventional gene therapy for cancer encounters challenges targeting tumor cells directly but delivering miRNA to the tumor stroma offers a straightforward and efficient means of altering the microenvironment, leading to substantial inhibition of tumor growth. AAV-mediated miR-29b delivery to peritoneum via IP route presents a simple, minimally invasive, and promising therapeutic strategy for refractory PM.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 12","pages":"1818-1830"},"PeriodicalIF":4.8,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399501","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

AAV-mediated combination gene therapy of inducible Caspase 9 and miR-199a-5p is therapeutic in hepatocellular carcinoma AAV介导的诱导型Caspase 9和miR-199a-5p联合基因疗法可治疗肝细胞癌。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-10-09 DOI: 10.1038/s41417-024-00844-x

Subhajit Pathak, Vijayata Singh, Narendra Kumar G., Giridhara R. Jayandharan

{"title":"AAV-mediated combination gene therapy of inducible Caspase 9 and miR-199a-5p is therapeutic in hepatocellular carcinoma","authors":"Subhajit Pathak, Vijayata Singh, Narendra Kumar G., Giridhara R. Jayandharan","doi":"10.1038/s41417-024-00844-x","DOIUrl":"10.1038/s41417-024-00844-x","url":null,"abstract":"Advanced-stage hepatocellular carcinoma (HCC) remains an untreatable disease with an overall survival of less than one year. One of the critical molecular mediators contributing to increased resistance to therapy and relapse, is increased hypoxia-inducible factor 1α (HIF-1α) levels, leading to metastasis of tumor cells. Several microRNAs are known to be dysregulated and impact HIF-1α expression in HCC. An in silico analysis demonstrated that hsa-miR-199a-5p is downregulated at various stages of HCC and is known to repress HIF-1α expression. Based on this analysis, we developed a combinatorial suicide gene therapy by employing hepatotropic Adeno-associated virus-based vectors encoding an inducible caspase 9 (iCasp9) and miR-199a. The overexpression of miR-199a-5p alone significantly decreased ( ~ 2-fold vs. Mock treated cells, p < 0.05) HIF-1α mRNA levels, with a concomitant increase in cancer cell cytotoxicity in Huh7 cells in vitro and in xenograft models in vivo. To further enhance the efficacy of gene therapy, we evaluated the synergistic therapeutic effect of AAV8-miR-199a and AAV6-iCasp9 in a xenograft model of HCC. Our data revealed that mice receiving combination suicide gene therapy exhibited reduced expression of HIF-1α ( ~ 4-fold vs. Mock, p < 0.001), with a significant reduction in tumor growth when compared to mock-treated animals. These findings underscore the therapeutic potential of downregulating HIF-1α during suicide gene therapy for HCC.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 12","pages":"1796-1803"},"PeriodicalIF":4.8,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388254","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

Systemic delivery of tannic acid-ferric-masked oncolytic adenovirus reprograms tumor microenvironment for improved therapeutic efficacy in glioblastoma 单宁酸-铁掩蔽的溶瘤腺病毒的全身给药可重塑肿瘤微环境，提高胶质母细胞瘤的疗效。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-10-09 DOI: 10.1038/s41417-024-00839-8

Guoqing Wang, Min Mu, Zongliang Zhang, Yongdong Chen, Nian Yang, Kunhong Zhong, Yanfang Li, Fang Lu, Gang Guo, Aiping Tong

{"title":"Systemic delivery of tannic acid-ferric-masked oncolytic adenovirus reprograms tumor microenvironment for improved therapeutic efficacy in glioblastoma","authors":"Guoqing Wang, Min Mu, Zongliang Zhang, Yongdong Chen, Nian Yang, Kunhong Zhong, Yanfang Li, Fang Lu, Gang Guo, Aiping Tong","doi":"10.1038/s41417-024-00839-8","DOIUrl":"10.1038/s41417-024-00839-8","url":null,"abstract":"Glioblastoma (GBM) represents the most aggressive primary brain tumor, and urgently requires effective treatments. Oncolytic adenovirus (OA) shows promise as a potential candidate for clinical antitumor therapy, including in the treatment of GBM. Nevertheless, the systemic delivery of OA continues to face challenges, leading to significantly compromised antitumor efficacy. In this study, we developed an innovative approach by encapsulating CXCL11-armed OA with tannic acid and Fe3+ (TA-Fe3+) to realize the systemic delivery of OA. The nanocarrier’s ability to protect the OA from elimination by host immune response was evaluated in vitro and in vivo. We evaluated the antitumor effect and safety profile of OA@TA-Fe3+ in a GBM-bearing mice model. OA@TA-Fe3+ effectively safeguarded the virus from host immune clearance and extended its circulation in vivo. After targeting tumor sites, TA-Fe3+ could dissolve and release Fe3+ and OA. Fe3+-induced O2 production from H2O2 relieved the hypoxic state, and promoted OA replication, leading to a remarkable alteration of tumor immune microenvironment and enhancement in antitumor efficacy. Moreover, the systemic delivery of OA@TA-Fe3+ was safe without inflammation or organ damage. Our findings demonstrated the promising potential of systemically delivering the engineered OA for effective oncolytic virotherapy against GBM.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 12","pages":"1-14"},"PeriodicalIF":4.8,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388265","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

Correction: PARD6A promotes lung adenocarcinoma cell proliferation and invasion through Serpina3 更正：PARD6A 通过 Serpina3 促进肺腺癌细胞增殖和侵袭。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-10-08 DOI: 10.1038/s41417-024-00840-1

Lanlin Hu, Mingxin Liu, Bo Tang, Xurui Li, Huasheng Xu, Huani Wang, Dandan Wang, Sijia Liu, Chuan Xu

引用次数: 0