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Retraction: MicroRNA-520b suppresses proliferation, migration, and invasion of spinal osteosarcoma cells via downregulation of frizzled-8. 撤回:MicroRNA-520b通过下调frizzled-8抑制脊柱骨肉瘤细胞的增殖、迁移和侵袭
IF 2 4区 医学
Oncology Research Pub Date : 2024-09-18 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056903
{"title":"Retraction: MicroRNA-520b suppresses proliferation, migration, and invasion of spinal osteosarcoma cells via downregulation of frizzled-8.","authors":"","doi":"10.32604/or.2024.056903","DOIUrl":"https://doi.org/10.32604/or.2024.056903","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504017X14873430389189.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1687-1688"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292716","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}
引用次数: 0
Retraction: LINC00052 promotes gastric cancer cell proliferation and metastasis via activating the Wnt/β-Catenin signaling pathway. 撤回:LINC00052通过激活Wnt/β-Catenin信号通路促进胃癌细胞增殖和转移
IF 2 4区 医学
Oncology Research Pub Date : 2024-09-18 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056891
{"title":"Retraction: LINC00052 promotes gastric cancer cell proliferation and metastasis via activating the Wnt/β-Catenin signaling pathway.","authors":"","doi":"10.32604/or.2024.056891","DOIUrl":"https://doi.org/10.32604/or.2024.056891","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504017X14897896412027.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1677-1678"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292709","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}
引用次数: 0
Retraction: MicroRNA 495 inhibits proliferation and metastasis and promotes apoptosis by targeting TWIST1 in gastric cancer cells. 撤回:MicroRNA 495 通过靶向 TWIST1 抑制胃癌细胞的增殖和转移并促进其凋亡
IF 2 4区 医学
Oncology Research Pub Date : 2024-09-18 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056898
{"title":"Retraction: MicroRNA 495 inhibits proliferation and metastasis and promotes apoptosis by targeting TWIST1 in gastric cancer cells.","authors":"","doi":"10.32604/or.2024.056898","DOIUrl":"https://doi.org/10.32604/or.2024.056898","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504018X15223159811838.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1681-1682"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292711","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}
引用次数: 0
Retraction: MicroRNA-107 promotes proliferation, migration, and invasion of osteosarcoma cells by targeting tropomyosin 1. 撤回:MicroRNA-107通过靶向肌球蛋白1促进骨肉瘤细胞的增殖、迁移和侵袭
IF 2 4区 医学
Oncology Research Pub Date : 2024-09-18 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056901
{"title":"Retraction: MicroRNA-107 promotes proliferation, migration, and invasion of osteosarcoma cells by targeting tropomyosin 1.","authors":"","doi":"10.32604/or.2024.056901","DOIUrl":"https://doi.org/10.32604/or.2024.056901","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504017X14882829077237.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1685-1686"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413829/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292713","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}
引用次数: 0
Retraction: miR-183 modulates cell apoptosis and proliferation in tongue squamous cell carcinoma SCC25 cell line. 撤稿:miR-183 可调节舌鳞状细胞癌 SCC25 细胞系的细胞凋亡和增殖。
IF 2 4区 医学
Oncology Research Pub Date : 2024-09-18 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056908
{"title":"Retraction: miR-183 modulates cell apoptosis and proliferation in tongue squamous cell carcinoma SCC25 cell line.","authors":"","doi":"10.32604/or.2024.056908","DOIUrl":"https://doi.org/10.32604/or.2024.056908","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504016X14685034103239.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1691-1692"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413823/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292717","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}
引用次数: 0
Exosomal microRNA let-7c-5p enhances cell malignant characteristics by inhibiting TAGLN in oral cancer. 外泌体 microRNA let-7c-5p 通过抑制口腔癌中的 TAGLN 增强细胞恶性特征。
IF 2 4区 医学
Oncology Research Pub Date : 2024-09-18 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.048191
Y I Li, Tianyi Wang, Haoran Ding, Shiyong Zhuang, Xiaobo Dai, Bing Yan
{"title":"Exosomal microRNA let-7c-5p enhances cell malignant characteristics by inhibiting TAGLN in oral cancer.","authors":"Y I Li, Tianyi Wang, Haoran Ding, Shiyong Zhuang, Xiaobo Dai, Bing Yan","doi":"10.32604/or.2024.048191","DOIUrl":"10.32604/or.2024.048191","url":null,"abstract":"<p><strong>Background: </strong>Oral cancer, a malignancy that is prevalent worldwide, is often diagnosed at an advanced stage. MicroRNAs (miRNAs) in circulating exosomes have emerged as promising cancer biomarkers. The role of miRNA let-7c-5p in oral cancer remains underexplored, and its potential involvement in tumorigenesis warrants comprehensive investigation.</p><p><strong>Methods: </strong>Serum samples from 30 patients with oral cancer and 20 healthy controls were used to isolate exosomes and quantify their RNA content. Isolation of the exosomes was confirmed through transmission electron microscopy. Quantitative PCR was used to assess the miRNA profiles. The effects of let-7c-5p and TAGLN overexpression on oral cancer cell viability, migration, and invasion were analyzed via CCK-8 and Transwell assays. Moreover, we conducted mRNA sequencing of exosomal RNA from exosomes overexpressing let-7c-5p to delineate the gene expression profile and identify potential let-7c-5p target genes.</p><p><strong>Results: </strong>let-7c-5p was upregulated in serum-derived exosomes of patients with oral cancer. Overexpression of let-7c-5p in the TCA8113 and CAL-27 cell lines enhanced their proliferative, migratory, and invasive capacities, and overexpression of let-7c-5p cell-derived exosomes promoted oral cancer cell invasiveness. Exosomal mRNA sequencing revealed 2,551 differentially expressed genes between control cell-derived exosomes and overexpressed let-7c-5p cell-derived exosomes. We further identified TAGLN as a direct target of let-7c-5p, which has been implicated in modulating the oncogenic potential of oral cancer cells. Overexpression of TAGLN reverses the promoting role of let-7c-5p on oral cancer cells.</p><p><strong>Conclusion: </strong>Our findings highlight the role of exosomal let-7c-5p in enhancing oral cancer cell aggressiveness by downregulating TAGLN expression, highlighting its potential as a diagnostic and therapeutic strategy.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1623-1635"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292791","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}
引用次数: 0
Metformin promotes anti-tumor immunity in STK11 mutant NSCLC through AXIN1-dependent upregulation of multiple nucleotide metabolites. 二甲双胍通过AXIN1依赖性上调多种核苷酸代谢物促进STK11突变NSCLC的抗肿瘤免疫。
IF 2 4区 医学
Oncology Research Pub Date : 2024-09-18 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.052664
Zhiguo Wang, Kunlin Li, Conghua Lu, Mingxia Feng, Caiyu Lin, Guofang Yin, Dan Luo, Wenyi Liu, Kaiyu Jin, Yuanyao Dou, D I Wu, Jie Zheng, Kejun Zhang, L I Li, Xianming Fan
{"title":"Metformin promotes anti-tumor immunity in <i>STK11</i> mutant NSCLC through AXIN1-dependent upregulation of multiple nucleotide metabolites.","authors":"Zhiguo Wang, Kunlin Li, Conghua Lu, Mingxia Feng, Caiyu Lin, Guofang Yin, Dan Luo, Wenyi Liu, Kaiyu Jin, Yuanyao Dou, D I Wu, Jie Zheng, Kejun Zhang, L I Li, Xianming Fan","doi":"10.32604/or.2024.052664","DOIUrl":"10.32604/or.2024.052664","url":null,"abstract":"<p><strong>Background: </strong>Metformin has pleiotropic effects beyond glucose reduction, including tumor inhibition and immune regulation. It enhanced the anti-tumor effects of programmed cell death protein 1 (PD-1) inhibitors in serine/threonine kinase 11 (<i>STK11)</i> mutant non-small cell lung cancer (NSCLC) through an axis inhibition protein 1 (AXIN1)-dependent manner. However, the alterations of tumor metabolism and metabolites upon metformin administration remain unclear.</p><p><strong>Methods: </strong>We performed untargeted metabolomics using liquid chromatography (LC)-mass spectrometry (MS)/MS system and conducted cell experiments to verify the results of bioinformatics analysis.</p><p><strong>Results: </strong>According to the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database, most metabolites were annotated into metabolism, including nucleotide metabolism. Next, the differentially expressed metabolites in H460 (refers to H460 cells), H460_met (refers to metformin-treated H460 cells), and H460_KO_met (refers to metformin-treated <i>Axin1</i> <sup><i>-/-</i></sup> H460 cells) were distributed into six clusters based on expression patterns. The clusters with a reversed expression pattern upon metformin treatment were selected for further analysis. We screened out metabolic pathways through KEGG pathway enrichment analysis and found that multiple nucleotide metabolites enriched in this pathway were upregulated. Furthermore, these metabolites enhanced the cytotoxicity of activated T cells on H460 cells <i>in vitro</i> and can activate the stimulator of the interferon genes (STING) pathway independently of AXIN1.</p><p><strong>Conclusion: </strong>Relying on AXIN1, metformin upregulated multiple nucleotide metabolites which promoted STING signaling and the killing of activated T cells in <i>STK11</i> mutant NSCLC, indicating a potential immunotherapeutic strategy for <i>STK11</i> mutant NSCLC.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1637-1648"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292793","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}
引用次数: 0
mRNA vaccines: a new era in vaccine development. mRNA 疫苗:疫苗开发的新时代。
IF 2 4区 医学
Oncology Research Pub Date : 2024-09-18 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.043987
Shubhra Chandra, Jennifer C Wilson, David Good, Ming Q Wei
{"title":"mRNA vaccines: a new era in vaccine development.","authors":"Shubhra Chandra, Jennifer C Wilson, David Good, Ming Q Wei","doi":"10.32604/or.2024.043987","DOIUrl":"10.32604/or.2024.043987","url":null,"abstract":"<p><p>The advent of RNA therapy, particularly through the development of mRNA cancer vaccines, has ushered in a new era in the field of oncology. This article provides a concise overview of the key principles, recent advancements, and potential implications of mRNA cancer vaccines as a groundbreaking modality in cancer treatment. mRNA cancer vaccines represent a revolutionary approach to combatting cancer by leveraging the body's innate immune system. These vaccines are designed to deliver specific mRNA sequences encoding cancer-associated antigens, prompting the immune system to recognize and mount a targeted response against malignant cells. This personalized and adaptive nature of mRNA vaccines holds immense potential for addressing the heterogeneity of cancer and tailoring treatments to individual patients. Recent breakthroughs in the development of mRNA vaccines, exemplified by the success of COVID-19 vaccines, have accelerated their application in oncology. The mRNA platform's versatility allows for the rapid adaptation of vaccine candidates to various cancer types, presenting an agile and promising avenue for therapeutic intervention. Clinical trials of mRNA cancer vaccines have demonstrated encouraging results in terms of safety, immunogenicity, and efficacy. Pioneering candidates, such as BioNTech's BNT111 and Moderna's mRNA-4157, have exhibited promising outcomes in targeting melanoma and solid tumors, respectively. These successes underscore the potential of mRNA vaccines to elicit robust and durable anti-cancer immune responses. While the field holds great promise, challenges such as manufacturing complexities and cost considerations need to be addressed for widespread adoption. The development of scalable and cost-effective manufacturing processes, along with ongoing clinical research, will be pivotal in realizing the full potential of mRNA cancer vaccines. Overall, mRNA cancer vaccines represent a cutting-edge therapeutic approach that holds the promise of transforming cancer treatment. As research progresses, addressing challenges and refining manufacturing processes will be crucial in advancing these vaccines from clinical trials to mainstream oncology practice, offering new hope for patients in the fight against cancer.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1543-1564"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292794","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}
引用次数: 0
IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway. IL13RA2通过激活糖酵解和Wnt/β-catenin信号通路促进婴儿血管瘤的进展。
IF 2 4区 医学
Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.048315
Ziyong Liu, Tao Ma, Jinfang Li, Wei Ren, Zhixin Zhang
{"title":"IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway.","authors":"Ziyong Liu, Tao Ma, Jinfang Li, Wei Ren, Zhixin Zhang","doi":"10.32604/or.2024.048315","DOIUrl":"10.32604/or.2024.048315","url":null,"abstract":"<p><strong>Background: </strong>Interleukin 13 receptor subunit alpha 2 (IL13RA2) plays an essential role in the progression of many cancers. However, the role of IL13RA2 in infantile haemangioma (IH) is still unknown.</p><p><strong>Materials and methods: </strong>IL13RA2 expression in IH tissues was analyzed using western blot, qRT-PCR, and immunofluorescence. The role of IL13RA2 in haemangioma-derived endothelial cells (HemECs) was determined following knockdown or overexpression of IL13RA2 using CCK-8, colony formation, apoptosis, wound healing, tubule formation, Transwell, and western blot.</p><p><strong>Results: </strong>IL13RA2 expression was upregulated in IH tissues. IL13RA2 overexpression promoted proliferation, migration, and invasion of HemECs and induced glycolysis, which was confirmed with a glycolysis inhibitor. Specifically, IL13RA2 interacted with β-catenin and activated the Wnt/β-catenin pathway in HemECs, which were involved in the above-mentioned effects of IL13RA2.</p><p><strong>Conclusions: </strong>These findings revealed that targeting IL13RA2 is a potential therapeutic approach for IH.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 9","pages":"1453-1465"},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110371","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}
引用次数: 0
Retraction: Knockdown of Long Noncoding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Inhibits Proliferation, Migration, and Invasion and Promotes Apoptosis by Targeting miR-124 in Retinoblastoma. 撤回:敲除长非编码 RNA (lncRNA) 转移相关肺腺癌转录本 1 (MALAT1) 通过靶向 miR-124 抑制视网膜母细胞瘤的增殖、迁移和侵袭并促进凋亡
IF 2 4区 医学
Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056121
{"title":"Retraction: Knockdown of Long Noncoding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Inhibits Proliferation, Migration, and Invasion and Promotes Apoptosis by Targeting miR-124 in Retinoblastoma.","authors":"","doi":"10.32604/or.2024.056121","DOIUrl":"https://doi.org/10.32604/or.2024.056121","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504017X14953948675403.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 9","pages":"1529"},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110378","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}
引用次数: 0
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