Oncology Research最新文献

{"title":"The SS18-SSX fusion oncoprotein: Friend and foe in targeted therapy for synovial sarcoma.","authors":"Gavin M Anchondo, Kyra Parker, Alexis Bruce, Elizabeth Cortez, L E Su","doi":"10.32604/or.2025.060573","DOIUrl":"https://doi.org/10.32604/or.2025.060573","url":null,"abstract":"<p><p>Synovial sarcoma is a high-grade soft tissue malignancy characterized by a unique fusion gene known as SS18-SSX. The SS18-SSX fusion protein acts as an oncogenic driver of synovial sarcoma, and it has thus been commonly accepted that disruption of SS18-SSX function represents a therapeutic means of treating synovial sarcoma, but emerging evidence suggests that upon depletion of SS18-SSX, an anti-apoptotic signal surprisingly arises to protect synovial sarcoma cell survival. In this article, we discuss the controversial roles of SS18-SSX's transcriptional activity in synovial sarcoma biology and outline a synergistic strategy for overcoming the resistance of synovial sarcoma cells to SS18-SSX targeted therapeutics.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 5","pages":"1001-1005"},"PeriodicalIF":2.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12033998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144003763","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":"Non-coding RNAs as potential mediators of resistance to lung cancer immunotherapy and chemotherapy.","authors":"Jiahui Wang, Hongcheng Ge, Zhengyuan Yu, Lingzhi Wu","doi":"10.32604/or.2024.058256","DOIUrl":"https://doi.org/10.32604/or.2024.058256","url":null,"abstract":"<p><p>Lung cancer is a common cause of cancer-related death globally. The majority of lung cancer patients initially benefit from chemotherapy and immunotherapy. However, as the treatment cycle progresses and the disease evolves, the emergence of acquired resistance leads to treatment failure. Many researches have shown that non-coding RNAs (ncRNAs) not only influence lung cancer progression but also act as potential mediators of immunotherapy and chemotherapy resistance in lung cancer, mediating drug resistance by regulating multiple targets and pathways. In addition, the regulation of immune response by ncRNAs is dualistic, forming a microenvironment for inhibits/promotes immune escape through changes in the expression of immune checkpoints. The aim of this review is to understand the effects of ncRNAs on the occurrence and development of lung cancer, focusing on the role of ncRNAs in regulating drug resistance of lung cancer.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 5","pages":"1033-1054"},"PeriodicalIF":2.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984908","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":"Current innovations in head and neck cancer: From diagnostics to therapeutics.","authors":"Tayyaba Sattar, Iqra Nazir, Mehreen Jabbar, Javaria Malik, Saba Afzal, Sana Hanif, Seyed Ali Mosaddad, Ahmed Hussain, Hamid Tebyaniyan","doi":"10.32604/or.2025.060601","DOIUrl":"https://doi.org/10.32604/or.2025.060601","url":null,"abstract":"<p><strong>Background: </strong>Head and neck cancers (HNC) account for a significant global health burden, with increasing incidence rates and complex treatment requirements. Traditional diagnostic and therapeutic approaches, while effective, often result in substantial morbidity and limitations in personalized care. This review provides a comprehensive overview of the latest innovations in diagnostics and therapeutic strategies for HNC from 2015 to 2024.</p><p><strong>Methods: </strong>A review of literature focused on pe-reviewed journals, clinical trial databases, and oncology conference proceedings. Key areas include molecular diagnostics, imaging technologies, minimally invasive surgeries, and innovative therapeutic strategies.</p><p><strong>Results: </strong>Technologies like liquid biopsy next-generation sequencing (NGS) have greatly improved diagnostic accuracy and personalization in HNC care. These advancements have improved survival rates and enhanced patients' quality of life. Personalized therapeutic approaches, including immune checkpoint inhibitors, precision radiation therapy, and surgery, have led to enhanced treatment efficacy while reducing side effects. The integration of AI and machine learning into diagnostics and treatment planning shows promise in optimizing clinical decision-making and predicting treatment outcomes.</p><p><strong>Conclusion: </strong>The current innovations in diagnostics and therapeutics are reshaping the management of head and neck cancer, offering more tailored and effective approaches to care. Overall, the continuous integration of these innovations in clinical practice is reshaping HNC treatment and improving patient outcomes and survival rates. Future research should focus on further refining these technologies, addressing challenges related to accessibility, and exploring their long-term clinical benefits in diverse patient populations.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 5","pages":"1019-1032"},"PeriodicalIF":2.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034008/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144032783","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: lncRNA FEZF1-AS1 Is Associated with Prognosis in Lung Adenocarcinoma and Promotes Cell Proliferation, Migration, and Invasion.","authors":"","doi":"10.32604/or.2025.065346","DOIUrl":"https://doi.org/10.32604/or.2025.065346","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504018X15199482824130.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 5","pages":"1251-1252"},"PeriodicalIF":2.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144022196","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":"Splicing factor PTBP1 promotes hepatocarcinogenesis via oncogenic splice-switching of MAPT.","authors":"Wenying Zheng, Yanyan Shang, Kai DU, Ailing Luo, Lijun Pei, Meiqi Li, Guoping Zhang, Min Deng","doi":"10.32604/or.2025.060958","DOIUrl":"https://doi.org/10.32604/or.2025.060958","url":null,"abstract":"<p><strong>Background: </strong>Alterations in splicing factors contribute to aberrant alternative splicing (AS), which subsequently promotes tumor progression. The splicing factor polypyrimidine tract binding protein 1 (PTBP1) has been shown to facilitate cancer progression by modulating oncogenic variants. However, its specific role and underlying mechanisms in hepatocellular carcinoma (HCC) remain to be elucidated.</p><p><strong>Methods: </strong>PTBP1 expression was evaluated in HCC tissues and cell lines. Subsequently, cells were transfected with vectors designed for PTBP1 overexpression or downregulation. The biological function of PTBP1 was assessed <i>in vitro</i> and <i>in vivo</i> using MTS assays, colony formation assays, transwell assays, xenograft formation, tail vein injection, and orthotopic models. Transcriptome analysis was conducted to elucidate the underlying molecular mechanisms.</p><p><strong>Results: </strong>Our findings demonstrated that PTBP1 exhibited elevated expression in HCC cell lines and tissues. Furthermore, its expression positively correlated with overall and disease-free survival rates, as well as tumor grade and stage. PTBP1 knockdown reduced HCC cell proliferation, migration, and invasion <i>in vitro</i> and suppressed hepatocarcinoma xenograft growth and infiltration <i>in vivo</i>. RNA sequencing (RNA-Seq) analysis identified the AS events associated with PTBP1. PTBP1 functionally enhanced cell proliferation, invasion, and migration by modulating the AS of the microtubule-associated protein tau (<i>MAPT</i>) gene and promoting oncogene expression. Notably, the dysregulation of MAPT splicing coincided with increased PTBP1 expression in HCC.</p><p><strong>Conclusions: </strong>PTBP1-guided AS of the <i>MAPT</i> gene enhances tumorigenicity in HCC through activation of the MAPK/ERK pathways.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 5","pages":"1121-1133"},"PeriodicalIF":2.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034000/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035594","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":"GlycoRNA: A new player in cellular communication.","authors":"Hyung Seok Kim","doi":"10.32604/or.2025.060616","DOIUrl":"https://doi.org/10.32604/or.2025.060616","url":null,"abstract":"<p><p>The discovery of glycosylated RNA molecules, known as glycoRNAs, introduces a novel dimension to cellular biology. This commentary explores the transformative findings surrounding glycoRNAs, emphasizing their unique roles in cancer progression and the therapeutic opportunities they present. GlycoRNAs, through interactions with lectins and immune receptors, may contribute to tumor immune evasion. Moreover, the therapeutic potential of this emerging knowledge includes interventions targeting glycoRNA synthesis and modulation of associated signaling pathways. By highlighting these critical insights, this commentary aims to encourage the development of innovative strategies that could improve cancer prognosis and treatment.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 5","pages":"995-1000"},"PeriodicalIF":2.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033055","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":"OTUB2 promotes proliferation and metastasis of triple-negative breast cancer by deubiquitinating TRAF6.","authors":"Y U Qiu, Ruihan Liu, Shanshan Huang, Qiaoting Cai, Y I Xie, Zhiting He, Weige Tan, Xinhua Xie","doi":"10.32604/or.2025.062767","DOIUrl":"https://doi.org/10.32604/or.2025.062767","url":null,"abstract":"<p><strong>Objectives: </strong>Deubiquitinase OTUB2 plays a critical role in the progression of various tumors. However, its specific role in triple-negative breast cancer (TNBC) remains unclear. This study aims to elucidate the biological function of OTUB2 in TNBC and uncover the underlying mechanisms.</p><p><strong>Methods: </strong>First, we found that the expression of <i>OTUB2</i> was upregulated in TNBC by bioinformatics analysis, we then validated its expression in TNBC tissues and cells using immunohistochemistry (IHC) and qPCR and plotted the survival curves by Kaplan-Meier method. Gene set enrichment analysis (GSEA) suggested that OTUB2 may be involved in tumor proliferation and metastasis. Further functional assays, including Cell Counting Kit-8 (CCK-8), colony formation, Transwell, and wound healing assays, were performed to assess the effects of OTUB2 overexpression and knockdown on TNBC cell proliferation and migration. Additionally, UbiBrowser 2.0 was used to identify OTUB2 substrate proteins and western blotting was conducted to clarify the molecular mechanisms involved.</p><p><strong>Results: </strong>Our results demonstrated that OTUB2 expression was elevated in TNBC and associated with poor prognosis. Overexpression of OTUB2 enhanced the proliferation and migration of TNBC cells, while its knockdown inhibited these processes. Moreover, OTUB2 stabilized tumor necrosis factor receptor-associated factor 6 (TRAF6) by deubiquitinating it, leading to activation of the protein kinase B (AKT) pathway.</p><p><strong>Conclusions: </strong>OTUB2 exerts its promoting effects on the progression of TNBC by activating the TRAF6/AKT pathway.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 5","pages":"1135-1147"},"PeriodicalIF":2.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034018/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144017936","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 synergistic antitumor effect of Karanahan technology and <i>in situ</i> vaccination using anti-OX40 antibodies.","authors":"Vera Ruzanova, Anastasia Proskurina, Genrikh Ritter, Evgeniya Dolgova, Sofya Oshikhmina, Svetlana Kirikovich, Evgeniy Levites, Yaroslav Efremov, Oleg Taranov, Alexandr Ostanin, Elena Chernykh, Nikolay Kolchanov, Sergey Bogachev","doi":"10.32604/or.2025.059411","DOIUrl":"https://doi.org/10.32604/or.2025.059411","url":null,"abstract":"<p><strong>Objectives: </strong>Currently, there exist two approaches to the treatment of malignant neoplasms: the Karanahan technology and <i>in situ</i> vaccination, which are based on chronometric delivery of therapeutic agents to the tumor depending on the characteristics of tumor cells, as well as the immune status. The main purpose of this study was to experimentally prove the feasibility of combining the Karanahan technology and <i>in situ</i> vaccination with αOX40 antibodies into a single therapeutic platform to achieve a potent additive antitumor therapeutic effect.</p><p><strong>Methods: </strong>BALB/c mice grafted with B-cellular lymphoma A20 were treated using the Karanahan technology consisting of intraperitoneal cyclophosphamide administrations and intratumoral DNA injections according to an individually determined therapeutic regimen, together with <i>in situ</i> vaccination with αOX40. A pathomorphological analysis of the organs of experimental animals that died during the initial attempt to combine the two technologies was carried out. An analysis of blood cell populations was performed to determine the safe time for antibody administration: the number of immune cells capable of activating systemic inflammation (CD11b+Ly-6C+, CD11b+Ly-6G+, CD3-NKp46+CD11b+), the presence of Fc receptor and OX40 on the surface of these cells, and the number of neutrophils activated to NETosis were analyzed. Based on the analysis results, the antitumor efficacy of various modes of combining the Karanahan technology and <i>in situ</i> vaccination was studied.</p><p><strong>Results: </strong>When αOX40 was administered 5 h after each treatment using the Karanahan technology, mass death of mice caused by systemic inflammation and multiple organ failure was observed. The state of blood cells after the treatment using the Karanahan technology at the time points corresponding to antibody injections was analyzed to elucidate the reasons for this effect. It was found that at some time points, there occurs activation of the immune system and a powerful release (up to 16%) of monocytes and granulocytes carrying Fc receptor and OX40 on their surface into blood; when interacting with αOX40, they can activate the lytic potential of these cells. Activation of neutrophils to NETosis was also observed. Based on these findings, a study was carried out in different time regimes to combine the Karanahan technology and αOX40 injections. When αOX40 was injected into the points of minimal release of myeloid cells into the blood, increased survival rate and the greatest antitumor efficacy were observed: 37% of animals survived without relapses on day 100 after experiment initiation. <b>Conclusions:</b> The results obtained indicate that it is possible to combine the Karanahan technology and <i>in situ</i> vaccination with αOX40, with obligatory constant monitoring of the number of myeloid cells in peripheral blood to determine the safe time for antibody injection.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 5","pages":"1229-1248"},"PeriodicalIF":2.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144046476","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 Wnt/β-catenin signaling gene signature for progression and metastasis of gastric cancer.","authors":"Jia Chen, Fei Jiang, Kaiyi Niu, Haodong Zhao, L I Li, Hongzhu Yu","doi":"10.32604/or.2024.054366","DOIUrl":"https://doi.org/10.32604/or.2024.054366","url":null,"abstract":"<p><strong>Backgrounds: </strong>As cancer progresses through various stages of malignancy, metastasis, and drug resistance, the Wnt/-catenin signaling is frequently dysregulated. Despite advancements in medical technology and therapeutic strategies, the prognosis for numerous gastric cancer patients remains unfavorable.</p><p><strong>Methods: </strong>For the analysis of prognostic signature genes associated with Wnt signaling in GC, we used LASSO (least absolute shrinkage and selection operator) regression. To explore the function, cell specificity, and transcriptional regulation of the signature gene Carboxypeptidase Z (CPZ), we conducted co-expression analysis, single-cell RNA sequencing data analysis, transcription factor prediction, and dual luciferase reporter assay. The knockdown and overexpression experiments were also performed to observe the changes in the downstream gene expression, as well as the influence on the biological functions of GC cells.</p><p><strong>Results: </strong>We identified a five-gene signature, including CPZ, Collagen Triple Helix Repeat Containing-1 (CTHRC1), Dickkopf-1 (DKK1), Epidermal Growth Factor (EGF), and Glypican Proteoglycan-3 (GPC3), with risk scores predictive of the prognosis of GC patients. We found that the adipocyte enhancer binding protein 1 (AEBP1) and transcription factor 3 (TCF3) could interact in the nucleus and synergistically enhance the expression of Wnt signaling-associated genes, including WNT2/FZD2 (Wnt family member 2/frizzled class receptor 2) and VIM (vimentin), thus promoting the invasion, migration, and malignant metastasis of GC.</p><p><strong>Conclusions: </strong>Our study offers a precise gene-signature prediction method for the prognosis of GC. We discovered the synergistic effect of AEBP1 and TCF3 in the nucleus on GC metastasis. GC may benefit from the identification of this potential therapeutic target.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 5","pages":"1199-1215"},"PeriodicalIF":2.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035189","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":"Promising roles of vitamin D receptor and APRO family proteins for the development of cancer stem cells targeted malignant tumor therapy.","authors":"Moeka Nakashima, Naoko Suga, Akari Fukumoto, Sayuri Yoshikawa, Satoru Matsuda","doi":"10.32604/or.2025.059657","DOIUrl":"https://doi.org/10.32604/or.2025.059657","url":null,"abstract":"<p><p>Malignant tumors are heterogeneous diseases characterized by uncontrolled cell proliferation, invasion, metastasis, and/or recurrence of their malignancies. In particular, cancer stem cells (CSCs) within these tumors might be responsible for the property of invasiveness and/or therapies-resistance. CSCs are a self-renewing, awfully tumorigenic subpopulation of cancer cells, which are notorious for strong chemoresistance and are frequently responsible the aggravated invasion, metastasis, and/or recurrence. Developing targeting therapies against CSCs, therefore, may be deliberated a more encouraging mission for the greater cancer therapy. Innovation for a more potent anti-CSC treatment has been required as soon as possible. Interestingly, vitamin D could modulate the inflammatory condition of the tumor microenvironment (TME) by successfully affecting CSCs, which has an imperative role in determining the malignant phenotype of CSCs. In addition, vitamin D may also contribute to the regulation of the malignant behaviors of CSCs. Consistently, vitamin D could have potential applications for the significant inhibition of several tumor growths within various cancer therapies. The biological significance of vitamin D for CSCs regulation may be involved in the function of APRO family proteins. Therefore, vitamin D could be one of the innovative therapeutic modalities for the development of novel CSCs related tumor therapies.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 5","pages":"1007-1017"},"PeriodicalIF":2.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144037822","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}