Oncology Research最新文献

{"title":"Retraction: Puerarin inhibits proliferation and induces apoptosis by upregulation of miR-16 in bladder cancer cell line T24.","authors":"","doi":"10.32604/or.2024.056915","DOIUrl":"https://doi.org/10.32604/or.2024.056915","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504018X15178736525106.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 4","pages":"993"},"PeriodicalIF":2.0,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11964883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795999","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":"The regulatory role of lncRNA in tumor drug resistance: refracting light through a narrow aperture.","authors":"Heng Zhang, Xiao Yang, Yujin Guo, Haibo Zhao, Pei Jiang, Qing-Qing Yu","doi":"10.32604/or.2024.053882","DOIUrl":"10.32604/or.2024.053882","url":null,"abstract":"<p><p>As living conditions improve and diagnostic capabilities advance, the incidence of tumors has increased, with cancer becoming a leading cause of death worldwide. Surgery, chemotherapy, and radiotherapy are the most common treatments. Despite advances in treatment options, chemotherapy remains a routine first-line treatment for most tumors. Due to the continuous and extensive use of chemotherapy drugs, tumor resistance often develops, becoming a significant cause of treatment failure and poor prognosis. Recent research has increasingly focused on how long stranded non-coding RNAs (LncRNAs) influence the development of malignant tumors and drug resistance by regulating gene expression and other biological mechanisms during cell growth. Studies have demonstrated that variations in lncRNA expression levels, influenced by both interpatient variability and intratumoral genetic and epigenetic differences, are closely linked to tumor drug resistance. Therefore, this review advocates using lncRNA as a framework to investigate the regulation of genes associated with drug resistance, proposing lncRNA-targeted therapeutic strategies to potentially increase the efficacy of chemotherapy, improve patient outcomes, and guide future research directions.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 4","pages":"837-849"},"PeriodicalIF":2.0,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11964869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143796041","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":"Cancer stem cell specificity as new targets in breast tumor treatment.","authors":"Zhizheng Zhang, Tao Li, Yuan Li, X I Wang, Hao Liu, Xinyu Shen, Ann Xu, Tiansong Xia, B O Xu","doi":"10.32604/or.2024.050505","DOIUrl":"10.32604/or.2024.050505","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer is a prevalent malignant tumor affecting females, with treatment options including surgery, radiotherapy, chemotherapy, and endocrine therapy.</p><p><strong>Methods: </strong>This review synthesizes existing literature on breast cancer stem cells and their applications in breast cancer treatment. PubMed, Web of Science, and other relevant databases were systematically searched using keywords such as \"breast cancer stem cells,\" \"immunotherapy,\" \"gene therapy,\" and \"cell therapy.\" Studies published in English were included, and their findings were analyzed to provide insights into the characteristics and therapeutic potential of breast cancer stem cells.</p><p><strong>Results: </strong>Breast cancer stem cells exhibit unique properties that contribute to tumor initiation, progression, recurrence, and therapy resistance. Immunotherapy targeting breast cancer stem cells shows promise in overcoming these challenges, but issues such as lack of specificity and drug resistance need to be addressed.</p><p><strong>Conclusions: </strong>Breast cancer stem cells represent promising targets for innovative therapeutic strategies aimed at improving treatment outcomes in breast cancer patients.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 4","pages":"811-819"},"PeriodicalIF":2.0,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11964876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795997","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":"The role of glutathione peroxidase 4 in the progression, drug resistance, and targeted therapy of non-small cell lung cancer.","authors":"Jiaheng Wei, Liangming Zhu","doi":"10.32604/or.2024.054201","DOIUrl":"10.32604/or.2024.054201","url":null,"abstract":"<p><p>Lung cancer is one of the main causes of cancer-related deaths globally, with non-small cell lung cancer (NSCLC) being the most prevalent histological subtype of lung cancer. Glutathione peroxidase 4 (GPX4) is a crucial antioxidant enzyme that plays a role in regulating ferroptosis. It is also involved in a wide variety of biological processes, such as tumor cell growth invasion, migration, and resistance to drugs. This study comprehensively examined the role of GPX4 in NSCLC and investigated the clinical feasibility of targeting GPX4 for NSCLC treatment. We discovered that GPX4 influences the progression of NSCLC by modulating multiple signaling pathways, and that blocking GPX4 can trigger ferroptosis and increase the sensitivity to chemotherapy. As a result, GPX4 represents a prospective therapeutic target for NSCLC. Targeting GPX4 inhibits the development of NSCLC cells and decreases their resistance to treatment.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 4","pages":"863-872"},"PeriodicalIF":2.0,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11964886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143796091","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":"<i>CYB5D2</i> inhibits the malignant progression of hepatocellular carcinoma by inhibiting <i>TGF-β</i> expression and epithelial-mesenchymal transition.","authors":"Dong Jiang, Zhi Qi, Zhiying Xu, Yiran Li","doi":"10.32604/or.2024.050125","DOIUrl":"10.32604/or.2024.050125","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is a prevalent liver malignancy. This study examined the roles of transforming growth factor beta (<i>TGF-β</i>) and cytochrome b5 domain containing 2 (<i>CYB5D2</i>) in HCC etiology and their prognostic biomarker potential.</p><p><strong>Methods: </strong>Key modules and prognostic genes were identified by analyzing the GSE101685 dataset by weighted gene co-expression network analysis (WGCNA) and Least absolute shrinkage and selection operator (LASSO) Cox regression. The expression levels of <i>CYB5D2</i> and <i>TGF-β</i> in HCC cell lines were quantified using Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting (WB) assays. Effects of <i>CYB5D2</i> overexpression on cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) marker regulation were assessed <i>in vitro</i>, while <i>in vivo</i> tumorigenicity was evaluated using a xenograft model of HCC in nude mice.</p><p><strong>Results: </strong>In this study, WGCNA identified the turquoise module as significantly associated with HCC, containing 452 DEGs. LASSO Cox regression analysis revealed 9 key prognostic genes, with <i>CYB5D2</i> being underexpressed in HCC cells and tissues. <i>TGF-β</i> was negatively correlated with <i>CYB5D2</i> expression, resulting in poor patient prognosis. Functional assays demonstrated that <i>CYB5D2</i> overexpression inhibited proliferation, migration, and invasion of HCC cell lines, and altered EMT marker expression. Furthermore, the addition of <i>TGF-β</i> partially reversed the suppressive effects caused by <i>CYB5D2</i> overexpression. <i>In vivo</i>, CYB5D2 overexpression significantly reduced tumor growth, indicating its potential as a therapeutic target for HCC.</p><p><strong>Conclusion: </strong>The tumor suppressor function of <i>CYB5D2</i> in HCC and its interaction with <i>TGF-β</i> offered fresh information on the molecular pathophysiology of HCC and possible treatment avenues.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"709-722"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663804","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 decorin in the development of oral mucosal carcinogenesis.","authors":"Yong Rao, Xiao Chen, Kaiyu Li, Minhai Nie, Xuqian Liu","doi":"10.32604/or.2024.053119","DOIUrl":"10.32604/or.2024.053119","url":null,"abstract":"<p><p>Decorin (DCN) is primarily found in the connective tissues of various parts of the body, including the lungs, kidneys, bone tissue, aorta, and tendons. It is an important component of the extracellular matrix (ECM) and belongs to the class I small leucine-rich proteoglycans family. DCN is increasingly attracting attention due to its significant role in tumors, fibrotic diseases, and the regulation of vascular formation. Moreover, its anti-tumor properties have positioned it as a promising biomarker in the fight against cancer. Numerous studies have confirmed that DCN can exert inhibitory effects in various solid tumors, particularly in oral squamous cell carcinoma (OSCC), by activating its downstream pathways through binding with the epidermal growth factor receptor (EGFR) and mesenchymal-epithelial transition (MET) receptor, or by stabilizing and enhancing the expression of the tumor suppressor gene p53 to mediate apoptosis in cancer cells that have undergone mutation. The occurrence of OSCC is a continuous and dynamic process, encompassing the transition from normal mucosa to oral potentially malignant disorders (OPMDs), and further progressing from OPMDs to the malignant transformation into OSCC. We have found that DCN may exhibit a bidirectional effect in the progression of oral mucosal carcinogenesis, showing a trend of initial elevation followed by a decline, which decreases with the differentiation of OSCC. In OPMDs, DCN exhibits high expression and may be associated with malignant transformation, possibly linked to the increased expression of P53 in OPMDs. In OSCC, the expression of DCN is reduced, which can impact OSCC angiogenesis, and inhibit tumor cell proliferation, migration, and invasion capabilities, serving as a potential marker for predicting adverse prognosis in OSCC patients. This article reviews the current research status of DCN, covering its molecular structure, properties, and involvement in the onset and progression of oral mucosal carcinogenesis. It elucidates DCN's role in this process and aims to offer insights for future investigations into its mechanism of action in oral mucosal carcinogenesis and its potential application in the early diagnosis and treatment of OSCC.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"577-590"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664128","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":"Oncogenic and tumor-suppressive roles of Lipocalin 2 (LCN2) in tumor progression.","authors":"Baoxing Huang, Zichang Jia, Chenchen Fu, Moxian Chen, Zezhuo Su, Yunsheng Chen","doi":"10.32604/or.2024.051672","DOIUrl":"10.32604/or.2024.051672","url":null,"abstract":"<p><p>Lipocalin-2 (LCN2) is a member of the lipocalin superfamily with multiple functions and can participate in the transport of a variety of small lipophilic ligands <i>in vivo</i>. LCN2 is significantly expressed in various tumors and plays an important role in regulating tumor cell proliferation, invasion, and metastasis. The specific actions of LCN2 in tumors may vary depending on the particular type of cancer involved. In this review, we provide an extensive overview of the transcriptional and post-transcriptional regulation of LCN2 in health and disease. Furthermore, we summarize the impact of LCN2 dysregulation in a broad range of tumors. Lastly, we examine the mechanisms of action of LCN2 during tumorigenesis, progression, and metastasis. Understanding the complex relationships between LCN2 and tumor development, progression, and metastasis is vital for advancing our knowledge of cancer biology, developing biomarkers for diagnosis and clinical decision-making, and creating therapeutic strategies to improve the management of patients with cancer.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"567-575"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915076/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664072","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-135a confers resistance to gefitinib in non-small cell lung cancer cells by upregulation of RAC1.","authors":"","doi":"10.32604/or.2024.056906","DOIUrl":"https://doi.org/10.32604/or.2024.056906","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504018X15166204902353.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"733"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664129","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":"A novel prognostic scoring model based on cuproptosis identifies COMMD1 as a novel therapy target for liver hepatocellular carcinoma.","authors":"K E Tian, Zhipeng Li, Xiangyu Zhai, Huaxin Zhou, Hui Yao","doi":"10.32604/or.2024.049772","DOIUrl":"10.32604/or.2024.049772","url":null,"abstract":"<p><strong>Background: </strong>Primary liver cancer poses a significant global health burden, with projections indicating a surpassing of one million cases by 2025. Cuproptosis, a copper-dependent mechanism of cell death, plays a crucial role in the pathogenesis, progression, and prognosis of various cancers, including hepatocellular carcinoma (HCC).</p><p><strong>Purpose: </strong>This study aimed to develop a prognostic model for HCC based on cuproptosis-related genes, utilizing clinical data and gene expression profiles from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases.</p><p><strong>Materials and methods: </strong>Clinical features and gene expression data of HCC patients were collected from publicly available databases. Patients from TCGA were randomly divided into training and testing sets, and Lasso Cox regression was applied to develop a predictive model using cuproptosis-related genes.</p><p><strong>Results: </strong>The analysis identified Copper Metabolism Domain Containing 1 (COMMD1) as a potential prognostic marker for HCC, with deletion of this gene impacting disease progression. Cellular functional experiments validated the role of COMMD1 in HCC.</p><p><strong>Conclusions: </strong>COMMD1 emerges as a promising candidate for HCC treatment, with implications for prognosis prediction and therapeutic targeting.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"617-630"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663807","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":"ICAT mediates the inhibition of stemness and tumorigenesis in acute myeloid leukemia cells induced by 1,25-(OH)₂D₃.","authors":"Yulian Wang, Lianli Zhu, Ronghao Zeng, Yunping Pu, Baijian Chen, Yuwei Tan, Ming Hong, Weijia Wang","doi":"10.32604/or.2024.051746","DOIUrl":"10.32604/or.2024.051746","url":null,"abstract":"<p><strong>Background: </strong>The role of 1,25-dihydroxyvitamin D3 (1,25-(OH)₂D₃) in cancer prevention and treatment is an emerging topic of interest. However, its effects on the stemness of acute myeloid leukemia (AML) cells are poorly understood.</p><p><strong>Methods: </strong>The proliferation and differentiation of AML cells (HL60 and NB4) were investigated by the CCK-8 assay, immunocytochemical staining, and flow cytometry. The abilities of HL60 and NB4 cells to form spheres were examined by the cell sphere formation assay. In addition, the levels of stemness-associated markers (SOX2, Nanog, OCT4, and c-Myc) in HL60 and NB4 cells were measured by western blotting and quantitative real-time polymerase chain reaction. Moreover, we obtained β-catenin-interacting protein 1 (ICAT)-knockout and ICAT-overexpressing HL-60 cells using gene editing and lentiviral infection techniques and investigated the role of ICAT in modulating the stemness-inhibiting effects of 1,25-(OH)₂D₃ using the aforementioned experimental methods. Finally, we validated our findings <i>in vivo</i> using NOD/SCID mice.</p><p><strong>Results: </strong>1,25-(OH)₂D₃ inhibited the proliferation and stemness of AML cells (HL60 and NB4) and induced their differentiation into monocytes. Additionally, the knockdown of ICAT in HL60 cells attenuated the inhibitory effects of 1,25-(OH)₂D₃ on proliferation and stemness and suppressed the expression of stemness markers. Conversely, overexpression of ICAT enhanced the aforementioned inhibitory effects of 1,25-(OH)₂D₃. Consistently, in NOD/SCID mice, 1,25-(OH)₂D₃ suppressed tumor formation by HL-60 cells, and the effects of ICAT knockdown or overexpression on 1,25-(OH)₂D₃ aligned with the <i>in vitro</i> findings.</p><p><strong>Conclusion: </strong>1,25-(OH)₂D₃ inhibits AML cell stemness, possibly through modulation of the ICAT-mediated Wnt/β-catenin signaling pathway.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 3","pages":"695-708"},"PeriodicalIF":2.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915073/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143664066","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}