Zhilan Zhang, Jie Zhou, Ruiru Huang, Xingxing Zhuang, Shoudong Ni
{"title":"Identification of CCNB1 as a biomarker for cellular senescence in hepatocellular carcinoma: a bioinformatics and experimental validation study.","authors":"Zhilan Zhang, Jie Zhou, Ruiru Huang, Xingxing Zhuang, Shoudong Ni","doi":"10.1007/s12672-025-02182-2","DOIUrl":"10.1007/s12672-025-02182-2","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC), originating in the liver and often asymptomatic in early stages, frequently metastasises and recures post-surgery. Currently, reliable diagnostic biomarkers and therapeutic targets for HCC are lacking. This study investigates the influence of cellular senescence on HCC, employing bioinformatics analysis and in vitro experiments to identify potential biomarkers.</p><p><strong>Methods: </strong>We integrated data from GEO microarrays (GSE14520, GSE45267 and GSE64041) to analyse differentially expressed genes (DEGs) using the R package limma. WGCNA identified gene modules highly correlated to HCC. Then, ageing-highly related differentially expressed genes (AgHDEGs) were identified. Correlation analysis, GO and KEGG functional enrichment analysis, and gene co-expression network analysis further elucidated the functions of AgHDEGs. The STRING database identified hub AgHDEGs with CCNB1 subsequently evaluated for diagnostic value using ROC curve analysis. Additionally, we explored the correlation between CCNB1 and immune cells and assessed its biological functions via GSEA. Ultimately, the conclusions from bioinformatics analysis were confirmed via in vitro experiments, complemented by molecular docking simulations of gene-drug interactions.</p><p><strong>Results: </strong>Eight AgHDEGs (KPNA2, CCT3, CCNB1, RACGAP1, CDKN3, FEN1, MT1X and FOXM1) were identified. PPI network analysis highlighted CCNB1 as hub AgHDEGs with ROC analysis confirming its strong diagnostic potential. Analysis of immune infiltration revealed a significant correlation between CCNB1 and M0 macrophages. Subsequent studies showed CCNB1's critical role in regulating the cell cycle. Validation experiments illustrated an upregulation of CCNB1 expression in HCC, while inhibiting CCNB1 may reduce HepG2 cell proliferation by promoting cellular senescence. Moreover, molecular docking indicated CCNB1 as a potential therapeutic target.</p><p><strong>Conclusion: </strong>Our study underscores CCNB1's potential impact on HCC senescence and progression, suggesting its candidacy as a biomarker for HCC.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"384"},"PeriodicalIF":2.8,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11933616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699968","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":"Histiocyte-rich rhabdomyoblastic tumor easily misdiagnosed as rhabdomyosarcoma: a case report.","authors":"Ting Xu, Shuai Luo","doi":"10.1007/s12672-025-02189-9","DOIUrl":"10.1007/s12672-025-02189-9","url":null,"abstract":"<p><strong>Background: </strong>Histiocyte-rich rhabdomyoblastic tumor (HRRMT) is an extremely rare tumor of uncertain origin. Morphologically, it closely resembles inflammatory leiomyosarcoma (ILMS) without smooth muscle differentiation, making clinical diagnosis particularly challenging. Due to its rarity, HRRMT is often misdiagnosed as rhabdomyosarcoma, leading to unnecessary aggressive treatment.</p><p><strong>Case presentation: </strong>A 62-year-old male was admitted to the hospital after an incidental discovery of a mass on his right thigh, first noticed seven days prior. Clinical examination revealed a well-circumscribed, painless mass measuring approximately 5 × 6 cm. Ultrasound and magnetic resonance imaging (MRI) suggested rhabdomyosarcoma in the distal sartorius muscle. However, histopathological analysis following surgical resection confirmed HRRMT. The patient did not undergo postoperative radiotherapy or chemotherapy, and no recurrence was observed during six months of follow-up.</p><p><strong>Conclusions: </strong>HRRMT is a rare tumor with favorable biological behavior. Given its morphological overlap with ILMS and rhabdomyosarcoma, early and accurate diagnosis is essential to prevent overtreatment. Extensive surgical resection remains an effective therapeutic approach. We report a case of HRRMT that is easily misdiagnosed as rhabdomyosarcoma, which will be a valuable case.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"385"},"PeriodicalIF":2.8,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11933611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699944","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":"Cardiotoxicity induced by chemotherapy and immunotherapy in cancer treatment: a bibliometric analysis.","authors":"Xi Zhang, Yanfeng Xue, Mingyan Hao","doi":"10.1007/s12672-025-02146-6","DOIUrl":"10.1007/s12672-025-02146-6","url":null,"abstract":"<p><strong>Objective: </strong>New chemotherapy and immunotherapy agents have revolutionized cancer treatment, significantly improving patient survival rates and quality of life while extending lifespans. However, these therapies often come with severe side effects, particularly cardiotoxicity. Over the past few decades, this field has seen steady growth. To better understand current trends, research hotspots, and collaborative networks in this area, a bibliometric analysis of relevant literature was conducted.</p><p><strong>Methods: </strong>A comprehensive search was performed in the Web of Science for articles on cardiotoxicity induced by chemotherapy and immunotherapy in cancer treatment, published in SSCI and SCI-EXPANDED up to October 21, 2024. Using software tools such as GraphPad Prism, CiteSpace, and VOSviewer, we analyzed various parameters including publication year, countries, institutions, journals, authors, and references. Additionally, co-occurrence analyses, cooperation relationship assessments, co-citation networks, keyword maps, clustering analyses, and keyword emergence evaluations were conducted.</p><p><strong>Results: </strong>As of October 21, 2024, a total of 5290 articles from 5674 institutions and 27,528 authors across 114 countries and regions were collected. The annual publication frequency and rate steadily increased. The United States emerge as the leading country in terms of publication volume, with the University of Texas System being the most prolific and frequently cited institution. \"Breast Cancer Research and Treatment\" was among the journals with revelant publications. Notable contributors included Ky bonnie and Thavendiranathan Paaladinesh, while Cardinale D achieved the highest average citation count per publication. Current research hotspots included echocardiography, trastuzumab, doxorubicin, radiotherapy, myocarditis, and 5-fluorouracil. The trend suggests that cardiotoxicity is expected to play an increasingly critical role in chemotherapy and immunotherapy for cancer treatment.</p><p><strong>Conclusion: </strong>This study provides a bibliometric visualization analysis of cardiotoxicity induced by chemotherapy and immunotherapy in the cancer treatment. It highlights current developments, collaborative efforts, and research hotspots within this field, offering essential scientific reference value for Cardio-Oncology.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"376"},"PeriodicalIF":2.8,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11930912/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691427","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":"Cell death pathway regulation by fatty acid metabolism-related genes in neuroblastoma: a multi-omics analysis identifying CHD5 as a novel biomarker.","authors":"Yankun Chen, Junzhi Liu, Yubin Jia, Jiaxing Yang, Yan Jin, Yun Liu, Benfu Zhong, Qiang Zhao","doi":"10.1007/s12672-025-02088-z","DOIUrl":"10.1007/s12672-025-02088-z","url":null,"abstract":"<p><strong>Background: </strong>Neuroblastoma in children is commonly found as an extracranial solid tumor with poor prognosis in high-risk cases impeding successful treatment. While dysregulated cell death mechanisms and metabolic reprogramming are hallmarks of cancer progression, the interplay between fatty acid metabolism and cell death pathway regulation in neuroblastoma remains incompletely understood.</p><p><strong>Methods: </strong>Identifying molecular subtypes influenced by fatty acid metabolism were built by consensus clustering analysis. Independent prognostic genes were identified through random survival forest analysis, acquiring a novel risk signature. Risk signatures were validated internally and externally, and their independent prognostic value, immune landscape, and drug susceptibility were explored. The study systematically analyzed correlations between signature genes and seven major cell death pathways (apoptosis, pyroptosis, ferroptosis, autophagy, necroptosis, cuproptosis, and disulfidptosis), encompassing over 1,200 genes to comprehensively explore the intricate relationships between these molecular signatures and diverse cell death mechanisms. Gene Set Enrichment Analysis (GSEA) was performed to assess pathway-level associations. Utilizing a single-cell dataset of neuroblastoma samples, cells were categorized and labeled based on UMAP analysis. Feature map visualization was employed to display the expression level and allocation of specific genes across various cell populations. Validation of CHD5 expression in NB cells and tissues was confirmed through Western blotting and immunohistochemical staining.</p><p><strong>Results: </strong>The study identified 42 fatty acid metabolism key enzyme genes whose expression was significantly different within high-risk and non-high-risk neuroblastoma patients, by which acquiring two distinct prognostic clusters associated with fatty acid metabolism. A machine learning approach was used to select 4 hub genes (CHD5, TP63, XKR4, and CTAG1A) for the establishment of a fatty acid metabolism prognostic risk model. Cell death pathway analysis revealed that TP63 exhibited the strongest correlations across multiple death pathways, particularly with necroptosis (r = 0.684, p = 2.80e-23) and pyroptosis (r = 0.647, p = 3.12e-20), while XKR4 showed moderate correlations with autophagy (r = 0.398, p = 2.09e-07) and CHD5 displayed selective associations. High risk score and low risk score groups displayed notable variations in the immune microenvironment, characterized by reduced immune cell infiltration in the high group leading to immune escape, and conversely, heightened responsiveness of the low group to immune checkpoint blockade therapy. Single-cell dataset analysis highlighted significant expression of CHD5 in specific cell populations, suggesting its potential as a marker gene for neuroblastoma. Immunohistochemical staining revealed varying levels of CHD5 expression across different clinica","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"377"},"PeriodicalIF":2.8,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11930905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691428","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":"Gut microbiome, dietary habits, and prostate cancer: a two-step Mendelian randomization revealing the causal associations.","authors":"Junhua Guo, Ting Huang, Heran Zhou","doi":"10.1007/s12672-025-02172-4","DOIUrl":"10.1007/s12672-025-02172-4","url":null,"abstract":"<p><strong>Background: </strong>Recent studies suggest that diet fizzy drinks may contribute to prostate cancer (PCa) development. However, the causal effects between diet fizzy drinks and PCa and whether gut microbiota (GM) act as a mediator remain unclear.</p><p><strong>Methods: </strong>We conducted two-sample Mendelian Randomization (MR) analyses utilizing large-scale genome-wide association studies (GWAS) data from the UK Biobank, the MiBioGen consortium, and PCa-related datasets. The inverse-variance weighted (IVW) method was used to evaluate the causal effects of GM and dietary preferences on PCa risk. A mediation analysis was performed to investigate whether GM mediates the relationship between dietary factors and PCa risk.</p><p><strong>Results: </strong>Diet fizzy drink consumption was causally associated with reduced PCa risk (OR = 0.83, 95% CI: 0.70-0.99, P = 0.041) and decreased abundance of PCa-risk-related GM taxa (Negativicutes and Selenomonadales). Mediation analysis did not reveal a statistically significant mediation effect, with a mediation proportion of 16% (95% CI: - 0.06-0.37, P = 0.13).</p><p><strong>Conclusion: </strong>Consumption of diet fizzy drinks may reduce the risk of PCa, potentially through modulation of the GM; however, further studies are required to confirm these findings and clarify underlying mechanisms.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"375"},"PeriodicalIF":2.8,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11929656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691433","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}
Yaohao Liang, Tianyu Ruan, Jiaqian He, Ketuan Huang, Min Wei, Shengqiang Tan
{"title":"Long-term survival in a patient with ruptured advanced hepatocellular carcinoma treated with nutritional therapy combined with apatinib and camrelizumab: a case report.","authors":"Yaohao Liang, Tianyu Ruan, Jiaqian He, Ketuan Huang, Min Wei, Shengqiang Tan","doi":"10.1007/s12672-025-02099-w","DOIUrl":"10.1007/s12672-025-02099-w","url":null,"abstract":"<p><strong>Background: </strong>Spontaneous rupture is a fatal complication of advanced hepatocellular carcinoma (HCC) with an extremely poor prognosis. Although immune checkpoint inhibitors, targeted therapies, and nutritional therapy have shown potential in the treatment of advanced HCC, their combined efficacy in complex cases with high tumor burden complicated by rupture and bleeding remains unclear.</p><p><strong>Case description: </strong>A 54-year-old male patient was diagnosed with Barcelona Clinic Liver Cancer (BCLC) stage C HCC with high tumor burden, accompanied by a history of chronic hepatitis B and moderate malnutrition. After initial treatment with apatinib (500 mg/day) and nutritional therapy, the patient experienced HCC rupture. Following emergency transarterial embolization for hemostasis, the treatment regimen was adjusted to camrelizumab (200 mg/2 weeks) combined with reduced-dose apatinib (250 mg/day), along with continued nutritional support. After 17 months of treatment, the patient underwent hepatectomy, with pathological examination showing complete remission in the left liver. Postoperative adjuvant therapy included transarterial chemoembolization, nutritional therapy, targeted therapy, and individualized immunotherapy. As of the 4-year follow-up, the patients has good quality of life and has not experienced recurrence.</p><p><strong>Conclusion: </strong>This case showcases a multimodal treatment strategy for patients with advanced HCC with high tumor burden and rupture complications, integrating individualized immuno-targeted therapy, interventional treatment, and nutritional management and providing a possible approach for achieving a long-term survival. This comprehensive treatment method may offer new insights into improving the prognosis of patients with advanced HCC.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"378"},"PeriodicalIF":2.8,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11930898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691435","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}
Joseph Nhyira Obisi, Abike Ndidiamaka Josephine Abimbola, Oluwasegun Adesina Babaleye, Peter Kwame Atidoglo, Saviour God'swealth Usin, Eudora Obioma Nwanaforo, Faith Sutu Patrick-Inezi, Ilemobayo Victor Fasogbon, Joseph Chimezie, Christianah Adebimpe Dare, Oluwadoyinsayemi Oluwadamilare Kuti, Daniel Ejim Uti, Humphrey Chukwudi Omeoga
{"title":"Unveiling the future of cancer stem cell therapy: a narrative exploration of emerging innovations.","authors":"Joseph Nhyira Obisi, Abike Ndidiamaka Josephine Abimbola, Oluwasegun Adesina Babaleye, Peter Kwame Atidoglo, Saviour God'swealth Usin, Eudora Obioma Nwanaforo, Faith Sutu Patrick-Inezi, Ilemobayo Victor Fasogbon, Joseph Chimezie, Christianah Adebimpe Dare, Oluwadoyinsayemi Oluwadamilare Kuti, Daniel Ejim Uti, Humphrey Chukwudi Omeoga","doi":"10.1007/s12672-025-02102-4","DOIUrl":"10.1007/s12672-025-02102-4","url":null,"abstract":"<p><p>Cancer stem cells (CSCs), are a critical subpopulation within tumours, and are defined by their capacity for self-renewal, differentiation, and tumour initiation. These unique traits contribute to tumour progression, metastasis, and resistance to conventional treatments like chemotherapy and radiotherapy, often resulting in cancer recurrence and poor patient outcomes. As such, CSCs have become focal points in developing advanced cancer therapies. This review highlights progress in CSC-targeted treatments, including chimeric antigen receptor T-cell (CAR-T) therapy, immunotherapy, molecular targeting, and nanoparticle-based drug delivery systems. Plant-derived compounds and gene-editing technologies, such as clustered regularly interspaced short palindromic repeats (CRISPR), are explored for their potential to enhance precision and minimize side effects. Metabolic pathways integral to CSC survival, such as mitochondrial dynamics, mitophagy (regulated by dynamin-related protein 1 [DRP1] and the PINK1/Parkin pathway), one-carbon metabolism, amino acid metabolism (involving enzymes like glutaminase (GLS) and glutamate dehydrogenase (GDH]), lipid metabolism, and hypoxia-induced metabolic reprogramming mediated by hypoxia-inducible factors (HIF-1α and HIF-2α), are examined as therapeutic targets. The adaptability of CSCs through autophagy, metabolic flexibility, and epigenetic regulation by metabolites like α-ketoglutarate, succinate, and fumarate is discussed. Additionally, extracellular vesicles and nicotinamide adenine dinucleotide (NAD⁺) metabolism are identified as pivotal in redox balance, DNA repair, and epigenetic modifications. Addressing challenges such as tumour heterogeneity, immune evasion, and treatment durability requires interdisciplinary collaboration. Advancing CSC-targeted therapies is essential for overcoming drug resistance and preventing cancer relapse, paving the way for transformative cancer treatments. This review underscores the importance of leveraging innovative technologies and fostering collaboration to revolutionize cancer treatment.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"373"},"PeriodicalIF":2.8,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11929669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691454","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":"Lower cytoplasmic expression of DDIT4 is associated with poor prognosis in gastric cancer patients.","authors":"Masoumeh Dehghan Manshadi, Fatemeh Tajik, Leili Saeednejad Zanjani, Farideh Hashemi, Mandana Rahimi, Fahimeh Fattahi, Sadegh Safaei, Zahra Madjd, Roya Ghods","doi":"10.1007/s12672-025-02065-6","DOIUrl":"10.1007/s12672-025-02065-6","url":null,"abstract":"<p><strong>Introduction: </strong>DNA damage-inducible transcript 4 (DDIT4), also known as Redd1, Dig2, and RTP801 was identified to be upregulated in response to a variety of cellular stresses, including DNA damage, endoplasmic reticulum stress, and energy stress. Several studies have discovered that dysregulation of DDIT4 involved in various cancers with paradoxical expression and roles. Hence, this study was designed to investigate the clinical significance and prognostic value of DDIT4 in different subtypes of gastric cancer (GC).</p><p><strong>Materials and methods: </strong>To evaluate the expression pattern of DDIT4 in GC tissues as well as adjacent normal tissue, we utilized immunohistochemistry on tissue microarray (TMA) slides.</p><p><strong>Results: </strong>Our findings revealed that nuclear expression of DDIT4 was higher in GC tissues than in non-malignant samples. Also, the cytoplasmic and membranous expression of DDIT4 were significantly lower in tumor samples (P = 0.007 and P = 0.002, respectively). The results indicated that there was a statistically significant association between low cytoplasmic and membranous expression of DDIT4 and advanced histological grade (P = 0.001 and P = 0.016). The survival analysis revealed that lowered cytoplasmic expression of DDIT4 is significantly associated with worse DSS (P = 0.038).</p><p><strong>Conclusion: </strong>Lower cytoplasmic expression of DDIT4 could serve as a promising prognostic biomarker in GC.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"374"},"PeriodicalIF":2.8,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11929655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691438","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}
Ming Li, Zhiliang Xu, Siqin Liang, Qiaoli Lv, Xiaoxiang You, Tinghao Yuan, Jun He, Qiang Tu
{"title":"Progress in ubiquitination and hepatocellular carcinoma: a bibliometric analysis.","authors":"Ming Li, Zhiliang Xu, Siqin Liang, Qiaoli Lv, Xiaoxiang You, Tinghao Yuan, Jun He, Qiang Tu","doi":"10.1007/s12672-025-02155-5","DOIUrl":"10.1007/s12672-025-02155-5","url":null,"abstract":"<p><strong>Background and purpose: </strong>Ubiquitination modifications can affect hepatocellular carcinoma (HCC) progression through various signaling pathways. However, no significant results have been observed regarding protein ubiquitination in HCC's therapeutic transformation. This study aimed to explore the research areas related to ubiquitination and HCC from a bibliometric perspective.</p><p><strong>Methods: </strong>Articles and reviews on HCC and ubiquitination published between 2000 and 2023 were obtained from the Web of Science Core Collection (WOSCC). CiteSpace, VOSviewer, and R-bibliometrix were used for the bibliometric and visualization analyses.</p><p><strong>Results: </strong>Altogether, 358 papers on ubiquitination and HCC were extracted from the WOSCC. Over 24 years, the number of publications has increased. Since the beginning of 2019, studies related to this topic have increased significantly, indicating that the role of ubiquitination modification in HCC is currently popular. China is the leading country in this field with the largest number of publications. The Chinese Academy of Sciences is one of the most influential institutions. Qiao, Yongxia, and Zhang Jie are highly productive authors with major achievements. The journal Cell Death & Disease had the highest number of publications, and the most highly cited journal was Oncogene. The highest citation burst intensity was Sung (2021). In the keyword strategy map, \"cancer antigens\" are popular keywords in HCC and ubiquitination research.</p><p><strong>Conclusion: </strong>A comprehensive visual analysis of ubiquitination and HCC research was conducted using bibliometric methods, showing the publications and popular topics in this field over the past two decades, thus providing references for the future direction of ubiquitination and HCC research.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"371"},"PeriodicalIF":2.8,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673427","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":"Causal role of immune cells in head and neck squamous cell carcinoma.","authors":"Panshu Xu, Zhenxing Zhang, Haoran Zhu, Conglin Hu, Yukang Ying","doi":"10.1007/s12672-025-02135-9","DOIUrl":"10.1007/s12672-025-02135-9","url":null,"abstract":"<p><p>Chronic inflammation, immune cell infiltration, and metabolic reprogramming play a crucial role in the development of head and neck squamous cell carcinoma (HNSCC). Based on the summary-level data from a genome-wide association study (GWAS), this study used Mendelian randomization (MR) analysis to investigate the causal relationship between immune cell phenotype and HNSCC. Two-step MR was employed to quantify the proportion of the effect of metabolite-mediated immunophenotypes on HNSCC. 16 immune phenotypes exhibited a causal relationship with HNSCC. HLA DR + CD4 + AC (OR: 1.31, 95% CI 1.07-1.59, P < 0.01) and EM CD8br AC cells (OR: 1.36, 95% CI 1.14-1.62, P < 0.01) showed the most significant P values. 13 metabolites have a causal relationship with HNSCC (P < 0.05). The proportion of the effect of Bilirubin degradation product, C16H18N2O5 (3) levels-mediated HLA DR + CD4 + AC on HNSCC was 7.17% (95% CI 1.04%-13.3%), while the proportion of the effect of Glutamine to alanine ratio-mediated EM CD8br AC on HNSCC was 8.88% (95% CI 2.2%-15.6%). Moreover, single-cell RNA-sequencing analysis confirmed that HLA DR + CD4 + AC and EM CD8br AC cells were commonly present in the HNSCC tumor microenvironment (TME). High expression of two immune phenotypes indicated a poorer prognosis. The results of differentially expressed genes (DEGs) analysis and functional enrichment indicated that Interferon-induced protein with tetratricopeptide repeats 1 (IFIT1)/Follicular dendritic cell secreted protein (FDCSP) and Keratin 19 type I (KRT19)/Kallikrein-related peptidase 5 (KLK5) may be responsible genes for two immune phenotypes, respectively. The results of quantitative real-time polymerase chain reaction (qRT-PCR) and survival analysis showed that FDCSP was significantly downregulated in HNSCC and could exert a protective effect. Collectively, our study clarified the causal relationship between immune cells, metabolites, and HNSCC, providing new insight for clinical diagnosis and treatment of HNSCC.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"372"},"PeriodicalIF":2.8,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676767","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}