Oncology Research最新文献

{"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> ^<i>-/-</i> 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}

{"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}

{"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}

{"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}

{"title":"Correction: Long non-coding RNA LINC02163 accelerates malignant tumor behaviors in breast cancer by regulating the microRNA-511-3p/HMGA2 axis as a competing endogenous RNA.","authors":"Chenglin Qin, Linfang Jin, Jia Li, Wenzhang Zha, Huiming Ding, Xiaorong Liu, Xun Zhu","doi":"10.32604/or.2024.051893","DOIUrl":"https://doi.org/10.32604/or.2024.051893","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3727/096504020X15928179818438.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 9","pages":"1517-1522"},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunomodulatory and chemopreventive effects of resveratrol on the digestive system cancers.","authors":"Meir Djaldetti","doi":"10.32604/or.2024.049745","DOIUrl":"10.32604/or.2024.049745","url":null,"abstract":"<p><p>Resveratrol (RSV), the primary polyphenol found in grapes, has been revealed to have anti-inflammatory properties by reducing the capacity of the peripheral blood mononuclear cells to produce pro-inflammatory cytokines, including IL-1β, IL-6, IL-1ra and TNFα. Considering the close association between chronic inflammation and cancer development, RSV's immunomodulatory properties are one way by which the polyphenol may inhibit cancer initiation, proliferation, neovascularization, and migration. Resveratrol influences the generation of microtumor environment which is one of the key factors in cancer progress. In addition to immunomodulation, RSV inhibits cancer development by expressing anti-oxidant effects, causing cell cycle arrest, stimulating the function of certain enzymes, and activating cell signaling pathways. The end outcome is one of the various forms of cell death, including apoptosis, pyroptosis, necroptosis, and more, as it has been observed <i>in vitro</i>. RSV has been shown to act against cancer in practically every organ, while its effects on colon cancer have been documented more frequently. It is remarkable that longer-term clinical studies that may have established the potential for this natural substance to serve as a therapeutic adjuvant to traditional anti-cancer medications were not prompted by the encouraging outcomes seen with cancer cells treated with non-toxic doses of resveratrol. The current review aims to assess the recent findings about the immunological and anti-cancer characteristics of RSV, with a particular emphasis on cancers of the digestive tract, as a challenge for future clinical research that may contribute to the better prognosis of cancer.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 9","pages":"1389-1399"},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NCAPD2 serves as a potential prognostic biomarker for lung adenocarcinoma and promotes cell proliferation, migration, invasion and cell cycle <i>in vitro</i>.","authors":"Peiling Wu, Lifang Zhao, Hongyan Zhang, Yueyan Lou, Dongfang Chen, Shan Xue, Xueqing Liu, Handong Jiang","doi":"10.32604/or.2024.047490","DOIUrl":"10.32604/or.2024.047490","url":null,"abstract":"<p><strong>Objectives: </strong>The pro-oncogenic effects of NCAPD2 have been extensively studied across various tumor types; however, its precise role within the context of lung adenocarcinoma (LUAD) remains elusive. This study aims to elucidate the biological functions of NCAPD2 in LUAD and unravel the underlying mechanistic pathways.</p><p><strong>Methods: </strong>Utilizing bioinformatics methodologies, we explored the differential expression of NCAPD2 between normal and tumor samples, along with its correlations with clinical-pathological characteristics, survival prognosis, and immune infiltration.</p><p><strong>Results: </strong>In the TCGA-LUAD dataset, tumor samples demonstrated significantly elevated levels of NCAPD2 expression compared to normal samples (<i>p</i> < 0.001). Clinically, higher NCAPD2 expression was notably associated with advanced T, N, and M stages, pathologic stage, gender, smoking status, and diminished overall survival (OS). Moreover, differentially expressed genes (DEGs) associated with NCAPD2 were predominantly enriched in pathways related to cell division. Immune infiltration analysis revealed that NCAPD2 expression levels were linked to the infiltration of memory B cells, naïve CD4+ T cells, activated memory CD4+ T cells, and M1 macrophages. <i>In vitro</i> experiments demonstrated that silencing NCAPD2 suppressed LUAD cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and cell cycle progression.</p><p><strong>Conclusions: </strong>In summary, NCAPD2 may represent a promising prognostic biomarker and novel therapeutic target for LUAD.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 9","pages":"1439-1452"},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: miR-181a-5p Promotes Proliferation and Invasion and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A).","authors":"","doi":"10.32604/or.2024.056126","DOIUrl":"https://doi.org/10.32604/or.2024.056126","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504017X14982569377511.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 9","pages":"1539"},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: miR-3188 Regulates Cell Proliferation, Apoptosis, and Migration in Breast Cancer by Targeting TUSC5 and Regulating the p38 MAPK Signaling Pathway.","authors":"","doi":"10.32604/or.2024.056118","DOIUrl":"https://doi.org/10.32604/or.2024.056118","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504017X14953948675421.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 9","pages":"1523"},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: miR-940 Upregulation Suppresses Cell Proliferation and Induces Apoptosis by Targeting PKC-δ in Ovarian Cancer OVCAR3 Cells.","authors":"","doi":"10.32604/or.2024.056127","DOIUrl":"https://doi.org/10.32604/or.2024.056127","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504016X14732772150145.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 9","pages":"1541"},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110385","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}