Oncology ResearchPub Date : 2024-09-18eCollection Date: 2024-01-01DOI: 10.32604/or.2024.047893
Egor V Batorov, Alisa D Ineshina, Tatiana A Aristova, Vera V Denisova, Svetlana A Sizikova, Daria S Batorova, Galina Y Ushakova, Ekaterina Y Shevela, Elena R Chernykh
{"title":"PD-1<sup>+</sup> and TIM-3<sup>+</sup> T cells widely express common γ-chain cytokine receptors in multiple myeloma patients, and IL-2, IL-7, IL-15 stimulation up-regulates PD-1 and TIM-3 on T cells.","authors":"Egor V Batorov, Alisa D Ineshina, Tatiana A Aristova, Vera V Denisova, Svetlana A Sizikova, Daria S Batorova, Galina Y Ushakova, Ekaterina Y Shevela, Elena R Chernykh","doi":"10.32604/or.2024.047893","DOIUrl":"10.32604/or.2024.047893","url":null,"abstract":"<p><strong>Background: </strong>Immune checkpoint ligand-receptor interactions appear to be associated with multiple myeloma (MM) progression. Simultaneously, previous studies showed the possibility of PD-1 and TIM-3 expression on T cells upon stimulation with common γ-chain family cytokines <i>in vitro</i> and during homeostatic proliferation. The aim of the present work was to study the impact of homeostatic proliferation on the expansion of certain T cell subsets up-regulating PD-1 and TIM-3 checkpoint molecules.</p><p><strong>Methods: </strong>The expression of CD25, CD122, CD127 common γ-chain cytokine receptors, phosphorylated signal transducer and activator of transcription-5 (pSTAT5) and eomesodermin (EOMES) was comparatively assessed with flow cytometry in PD-1- and TIM-3-negative and positive T cells before the conditioning and during the first post-transplant month in peripheral blood samples of MM patients.</p><p><strong>Results: </strong>Substantial proportions of PD-1- and TIM-3-positive T lymphocytes expressed common γ-chain cytokine receptors and pSTAT5. Frequencies of cytokine receptor expressing cells were significantly higher within TIM-3<sup>+</sup> T cells compared to PD-1<sup>+</sup>TIM-3<sup>-</sup> subsets. Considerable proportions of both PD-1-/TIM-3-negative and positive CD8<sup>+</sup> T cells express EOMES, while only moderate frequencies of CD4<sup>+</sup> PD-1<sup>+</sup>/TIM-3<sup>+</sup> T cells up-regulate this transcription factor. Besides, the surface presence of CD25 and intranuclear expression of EOMES in CD4<sup>+</sup> T cells were mutually exclusive regardless of PD-1 and TIM-3 expression. The stimulation with common γ-chain cytokines up-regulates PD-1 and TIM-3 during the proliferation of initially PD-1/TIM-3-negative T cells but fails to expand initially PD-1<sup>+</sup> and TIM-3<sup>+</sup> T cell subsets <i>in vitro</i>.</p><p><strong>Conclusions: </strong>Both PD-1 and TIM-3 expressing T cells appear to be able to respond to homeostatic cytokine stimulation. Differences in common γ-chain cytokine receptor expression between PD-1<sup>+</sup> and TIM-3<sup>+</sup> T cells may reflect functional dissimilarity of these cell subsets. Checkpoint blockade appears to alleviate lymphopenia-induced proliferation of PD-1<sup>+</sup> T cells but may raise the possibility of immune-mediated adverse events.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1575-1587"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413821/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292796","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}
Oncology ResearchPub Date : 2024-09-18eCollection Date: 2024-01-01DOI: 10.32604/or.2024.056894
{"title":"Retraction: Long noncoding RNA CAMTA1 promotes proliferation and mobility of the human breast cancer cell line MDA-MB-231 via targeting miR-20b.","authors":"","doi":"10.32604/or.2024.056894","DOIUrl":"https://doi.org/10.32604/or.2024.056894","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504017X14953948675395.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1679-1680"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292710","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}
Oncology ResearchPub Date : 2024-09-18eCollection Date: 2024-01-01DOI: 10.32604/or.2024.056919
{"title":"Retraction: miRNA-497 negatively regulates the growth and motility of chondrosarcoma cells by targeting Cdc25A.","authors":"","doi":"10.32604/or.2024.056919","DOIUrl":"https://doi.org/10.32604/or.2024.056919","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504016X14519157902681.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1699-1700"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292719","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}
Oncology ResearchPub Date : 2024-09-18eCollection Date: 2024-01-01DOI: 10.32604/or.2024.047933
Weigang Xiu, Xingyu Liu, Kaixin Hu, Qin Zhang, Huashan Shi
{"title":"The role of cholesterol metabolism in lung cancer.","authors":"Weigang Xiu, Xingyu Liu, Kaixin Hu, Qin Zhang, Huashan Shi","doi":"10.32604/or.2024.047933","DOIUrl":"10.32604/or.2024.047933","url":null,"abstract":"<p><p>Elevated serum cholesterol metabolism is associated with a reduced risk of lung cancer. Disrupted cholesterol metabolism is evident in both lung cancer patients and tumor cells. Inhibiting tumor cell cholesterol uptake or biosynthesis pathways, through the modulation of receptors and enzymes such as liver X receptor and sterol-regulatory element binding protein 2, effectively restrains lung tumor growth. Similarly, promoting cholesterol excretion yields comparable effects. Cholesterol metabolites, including oxysterols and isoprenoids, play a crucial role in regulating cholesterol metabolism within tumor cells, consequently impacting cancer progression. In lung cancer patients, both the cholesterol levels in the tumor microenvironment and within tumor cells significantly influence cell growth, proliferation, and metastasis. The effects of cholesterol metabolism are further mediated by the reprogramming of immune cells such as T cells, B cells, macrophages, myeloid-derived suppressor cells, among others. Ongoing research is investigating drugs targeting cholesterol metabolism for clinical treatments. Statins, targeting the cholesterol biosynthesis pathway, are widely employed in lung cancer treatment, either as standalone agents or in combination with other drugs. Additionally, drugs focusing on cholesterol transportation have shown promise as effective therapies for lung cancer. In this review, we summarized current research regarding the rule of cholesterol metabolism and therapeutic advances in lung cancer.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1613-1621"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292722","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":"Research progress on the role of adipocyte exosomes in cancer progression.","authors":"Yun Wang, Xiaojiang Li, Dalong Liu, Zhifeng Wang, Jichen Xia, Lijun Wang, Xudong Zhang","doi":"10.32604/or.2024.043482","DOIUrl":"10.32604/or.2024.043482","url":null,"abstract":"<p><p>Exosomes, minute vesicles ubiquitously released by diverse cell types, serve as critical mediators in intercellular communication. Their pathophysiological relevance, especially in malignancies, has garnered significant attention. A meticulous exploration of the exosomal impact on cancer development has unveiled avenues for innovative and clinically valuable techniques. The cargo conveyed by exosomes exerts transformative effects on both local and distant microenvironments, thereby influencing a broad spectrum of biological responses in recipient cells. These membrane-bound extracellular vesicles (EVs) play a pivotal role in delivering bioactive molecules among cells and organs. Cellular and biological processes in recipient cells, ranging from stromal cell reprogramming to immunological responses, extracellular matrix formation, and modulation of cancer cell activation, expansion, and metastasis, are subject to exosome-mediated cell-to-cell communication. Moreover, exosomes have been implicated in endowing cancer cells with resistance to treatment. Extensive research has explored the potential of exosomes as therapeutic targets and diagnostic indicators. This comprehensive review seeks to provide an in-depth understanding of the pivotal components and roles of exosomes in tumorigenesis, growth, progression, and therapeutic responses. The insights into the multifaceted involvement of exosomes in malignant cancers are essential for the scientific community, fostering the development of novel therapeutic and diagnostic strategies in the relentless pursuit of cancer.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1649-1660"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292707","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}
Oncology ResearchPub Date : 2024-09-18eCollection Date: 2024-01-01DOI: 10.32604/or.2024.056905
{"title":"Retraction: MicroRNA-1284 inhibits cell viability and induces apoptosis of ovarian cancer cell line OVCAR3.","authors":"","doi":"10.32604/or.2024.056905","DOIUrl":"https://doi.org/10.32604/or.2024.056905","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504016X14685034103518.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 10","pages":"1689-1690"},"PeriodicalIF":2.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292714","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}