Cellular Oncology最新文献

{"title":"Single-cell and bulk transcriptome analysis identifies B-cell subpopulations and associated cancer subtypes with distinct clinical and molecular characteristics.","authors":"Yin He, Li Zhao, Yufen Zheng, Xiaosheng Wang","doi":"10.1007/s13402-025-01082-5","DOIUrl":"https://doi.org/10.1007/s13402-025-01082-5","url":null,"abstract":"<p><strong>Backgroud: </strong>Previous studies have identified B cell subpopulations with pro- and anti-tumoral activities, while the clinical relevance of B cell subpopulations-specific markers in pan-cancer remains understudied.</p><p><strong>Methods: </strong>We integrated 14 scRNA-seq datasets (102,504 cells from 424 patients, 15 cancer types) to identify B cell subpopulations via unsupervised clustering. We characterized their functional dynamics and prognostic relevance through analyzing single-cell, bulk and spatial transcriptomic data. Moreover, using B cell subpopulations-specific gene signatures, we constructed models for predicting cancer prognosis and immunotherapy response.</p><p><strong>Results: </strong>We identified eight B cell subpopulations (b00-b07) which were classified into naive, plasma, memory, germinal center (GC), and cycling B cells. Trajectory analysis revealed b02-naive and b04-GC cells in early phases, evolving into b01- and b03-plasma/b05- and b06-memory/b07-cycling and b05-memory subpopulations. Anti-tumor responses were activated in early pseudotime, complement/immunoglobulin pathways peaked in mid-pseudotime, and energy metabolism increased in late-pseudotime. The enrichment of b07-cycling and b04-GC was negatively correlated with cancer prognosis, while b02-naive had a positive correlation. Spatial transcriptomic analysis showed clustered b00-b06 versus dispersed b07 cells, with b04-GC and b07-cycling cells distant from tertiary lymphoid structure cores. Based on the expression profiles of 1,047 B cell subpopulations-specific signatures, we identified three pan-cancer subtypes with distinct clinical and molecular characteristics. Using 13 B cell subpopulations-specific signatures, we constructed models to accurately predict cancer survival outcomes and immunotherapy response.</p><p><strong>Conclusions: </strong>Our study delineates eight B cell subpopulations with distinct prognostic relevance. Signature-based stratification and models underscore their clinical relevance in cancer outcomes and therapy response, advancing understanding of B cell heterogeneity in cancer.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactylation: the regulatory code of cellular life activity and a barometer of diseases.","authors":"Xuebing Xu, Xuming Wu, Dandan Jin, Jie Ji, Tong Wu, Mengxiang Huang, Junpeng Zhao, Zihan Shi, Lirong Zhou, XuYang He, Yuxuan Huang, Shihai Xuan, Mingbing Xiao, Xiaolei Cao","doi":"10.1007/s13402-025-01083-4","DOIUrl":"https://doi.org/10.1007/s13402-025-01083-4","url":null,"abstract":"<p><p>Lactylation is a novel post-translational modification of proteins, which has attracted extensive attention since its discovery. Lactylation takes lactate, a common metabolite, as its substrate and mediates the modification under the action of lactyltransferases. Although lactylation modification was initially found to undergo in histones, subsequent studies have shown that this novel modification is not limited to specific protein classes, and can undergo in both histone and non-histone proteins. Lactylation has been proved to play an important regulatory role in a variety of diseases, including tumors, metabolic disorders, cardiovascular diseases, and neurodegenerative diseases. Given the tumor properties of its substrate lactate, lactylation has been most extensively studied in tumors, and as a result, we have gained a deeper understanding of the potential molecular mechanisms and regulatory roles of lactylation in tumors. In this paper, we will summarize the regulatory and functional mechanisms of lactylation, explain the cellular processes in which lactylation is involved and its association with various diseases, and look forward to the future clinical application of lactylation.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of CDK4/6 Inhibition in colorectal cancer and the role of p16 expression in predicting drug resistance.","authors":"Julia S Schneider, Najib Ben Khaled, Liangtao Ye, Ralf Wimmer, Linda Hammann, Alexander Weich, Christoph Suppan, Ujjwal M Mahajan, Andreas Jung, Jörg Kumbrink, Gerald Denk, Monika Rau, Volker Kunzmann, Solveig Kuss, Jens Neuman, Julia Mayerle, Andreas Geier, Heike M Hermanns, Enrico N De Toni, Florian P Reiter","doi":"10.1007/s13402-025-01080-7","DOIUrl":"https://doi.org/10.1007/s13402-025-01080-7","url":null,"abstract":"<p><strong>Introduction: </strong>Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide. The use of sequential polychemotherapies has improved the survival of patients with advanced metastatic disease. However, the survival rates achieved are low, and chemotherapy-related side effects are significant. Therefore, new, efficient, and tolerable therapies are urgently needed. In this study, we investigate the efficacy of pharmacological cyclin D-dependent kinase (CDK) 4/6 inhibition and explore the relevance of p16 as predictors of susceptibility to CDK 4/6 therapy.</p><p><strong>Materials and methods: </strong>CDK 4/6 inhibitors were evaluated in native and FOLFOX- or ribociclib-resistant CRC, hepatocellular carcinoma (HCC), and breast cancer (BC) cell lines using viability, colony formation, and flow cytometry (FC)-based assays. Western blotting was employed to assess the expression of Rb and members of the INK4 family. SiRNA-based knockdown of CDK4/6 was utilized to gain insights into mechanisms of action or resistance. Tissue from 185 CRC patients was examined for the expression of p16 and its relevance for progression-free and overall survival. The prognostic relevance of cyclin-dependent kinase inhibitor 2 A (CDKN2A) mRNA expression data was derived from The Cancer Genome Atlas (TCGA) data.</p><p><strong>Results: </strong>Ribociclib demonstrates significant antitumoral effects in various CRC, HCC, and BC cell lines, similar to two other approved CDK4/6 inhibitors (palbociclib and abemaciclib). Ribociclib-resistant cell lines (Hep-3B, HCC-1937, and BT-549) exhibited higher p16 expression compared to ribociclib-sensitive cell lines. In ribociclib-sensitive cell lines, CDK4/6 inhibition led to G1 phase arrest, whereas resistant cells did not exhibit such effects. A similar phenotype could be observed upon dual siRNA based CDK4/6 knockdown in ribociclib-sensitive HuH-7 and ribociclib-resistant Hep-3B cell lines. All CRC cell lines tested showed sensitivity to ribociclib, including the FOLFOX-resistant SW620 cell line. Low mRNA expression of CDKN2A (p16) was associated with favorable prognosis in CRC patients. No prognostic significance was found for p16 protein expression in an early-stage CRC cohort (n = 185).</p><p><strong>Conclusion: </strong>Ribociclib demonstrates significant antitumoral effects across a large panel of cancer cell lines and chemoresistant models, especially in CRC. Resistance towards ribociclib is associated with high p16 expression, which is a negative prognostic marker for patients with CRC. Our findings underscore p16 as a promising biomarker for predicting ribociclib responsiveness and emphasize the need for further mechanistic studies and combination therapy approaches to overcome resistance in p16^high patients.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"OTUD1 downregulates PD-L1 expression by deubiquitinating STAT3 and promotes the immune response in CcRCC.","authors":"Huaiyuan Liang, Xinlin Liu, Wanyang Guo, Wei Xiong, Da Ren, Wentao Liu","doi":"10.1007/s13402-025-01079-0","DOIUrl":"https://doi.org/10.1007/s13402-025-01079-0","url":null,"abstract":"<p><strong>Background: </strong>Clear cell renal cell carcinoma (ccRCC) is the most common malignant tumor of the urinary system and has the highest mortality rate. In addition to surgical tumor reduction, systemic drug therapy is the most important treatment method for metastatic renal cancer. In recent years, immunotherapeutic drugs represented by PD-1 antibodies have been used in the treatment of metastatic ccRCC and achieved good therapeutic effects. However, due to the occurrence of immune escape, only about 50-60% of patients with advanced renal cancer can significantly benefit from immunotherapy. The mechanism of immune escape is extremely complex and has not been clarified. We intend to delve into the driving mechanisms of immune evasion in ccRCC and explore potential targets for intervention.</p><p><strong>Methods: </strong>In this study, we analyzed the expression of OTUD1 and related pathways in ccRCC through TCGA, GEO dataset, and cBioPortal web tool. At the same time, a mouse model of allogeneic transplanted clear cell renal cell carcinoma was constructed, and the effect of OTUD1 on anti-PD1 antibody therapy was discussed. Experiments such as co-IP, flow cytometry, and RNA-seq analysis were used to investigate the mechanism by which OTUD1 regulates immunity through STAT3.</p><p><strong>Results: </strong>This study reveals that OTUD1 suppresses PD-L1 expression and enhances antitumor immunity in clear cell renal cell carcinoma (ccRCC) by deubiquitinating and stabilizing STAT3, thereby inhibiting its nuclear translocation and transcriptional activity. As a key regulator of the JAK-STAT pathway, OTUD1 disrupts PD-1/PD-L1-mediated immune evasion, offering a potential therapeutic strategy to improve immunotherapy responses in ccRCC. These findings highlight the OTUD1-STAT3-PD-L1 axis as a novel mechanism for overcoming immune checkpoint resistance.</p><p><strong>Conclusion: </strong>Overall, we demonstrate that OTUD1 interacts with STAT3 and deubiquitinates, inhibits its nuclear translocation and activity, and ultimately inhibits immune evasion of ccRCC by downregulating PD-L1.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thymidine kinase 1 indicates resistance to immune checkpoint plus tyrosine kinase inhibition in renal cell carcinoma.","authors":"Jiajun Wang, Xianglai Xu, Ying Wang, Yanjun Zhu","doi":"10.1007/s13402-025-01048-7","DOIUrl":"10.1007/s13402-025-01048-7","url":null,"abstract":"<p><strong>Purpose: </strong>Immune checkpoint plus tyrosine kinase inhibition (IO + TKI) has emerged as the first-line therapy in metastatic renal cell carcinoma (RCC), but no biomarker can predict its efficacy. Thymidine kinase 1 (TK1) is closely associated with immune evasion in tumors.</p><p><strong>Methods: </strong>Metastatic RCC patients treated by IO + TKI were enrolled from two cohorts (ZS-MRCC, n = 45; Javelin-101, n = 726). High-risk localized RCC were also enrolled (ZS-HRRCC, n = 40). TK1 was assessed by RNA-sequencing in all cohorts, and the immune contexture was assessed by flow cytometry and immunohistochemistry.</p><p><strong>Results: </strong>Higher TK1 expression was found in patients resistant to IO + TKI therapy (p = 0.025). High-TK1 group showed poor progression-free survival (PFS) in both the ZS-MRCC cohort (P = 0.008) and the Javelin-101 cohort (P = 0.036). By multivariate Cox regression, high-TK1 was determined as an independent factor for poor PFS (hazard ratio (HR) = 3.855, P = 0.002). High-TK1 expression was associated with decreased granzyme B⁺ CD8⁺ T cells (ρ=-0.22, P = 0.18), increased PD1⁺ CD4⁺ T cells (ρ = 0.33, P = 0.04), increased PDL1⁺ macrophages (ρ = 0.45, P < 0.001), and increased regulatory T cells (ρ = 0.35, P = 0.03). A novel random forest (RF) risk score was built by machine learning based on TK1 and immunologic parameters. Combined IO + TKI therapy surpassed sunitinib monotherapy in the low RF risk score group (HR = 0.158, P < 0.001), but was inferior to sunitinib in the high RF risk score group (HR, 2.195, P < 0.001).</p><p><strong>Conclusion: </strong>High-TK1 expression could be a potential indicator for therapeutic resistance, poor PFS and immune evasion in metastatic RCC under IO + TKI therapy. The novel RF risk score may help stratify patients for IO + TKI therapy.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"775-787"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143499675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating the prognostic significance of tumor deposits in gastric cancer and strategies for their integration into the TNM staging system: a single-center retrospective study.","authors":"Jun Yu, Ruirong Yao, Ning Han, Linbin Lu, Ling Chen, Abudurousuli Reyila, Xinlin Wang, Junya Yan, Shibo Wang, Yong Guo, Qingchuan Zhao, Kaichun Wu, Yuanyuan Lu, Gang Ji, Zengshan Li, Xianchun Gao, Yongzhan Nie","doi":"10.1007/s13402-025-01046-9","DOIUrl":"10.1007/s13402-025-01046-9","url":null,"abstract":"<p><strong>Purpose: </strong>To propose a new optimal strategy for incorporating tumor deposit (TD) into TNM staging.</p><p><strong>Methods: </strong>Totally, 2730 consecutive gastric cancer (GC) patients were included according to the presence and count of TDs between January 2011 and December 2014. Overall survival (OS) was analyzed using Cox regression and propensity score matching (PSM). The relationship between the number of TDs and GC patients' prognosis was analyzed using restricted cubic spline curves and compared with the prognostic value of lymph node metastases (LNMs). Harrell's C-index (C-index) and the Akaike information criterion (AIC) were employed to assess the prognostic performance of different staging systems.</p><p><strong>Results: </strong>The positive rate of TD was 9.67% (264/2730). The presence of TD was associated with poorer OS before PSM (hazard ratio (HR): 3.31; 95% confidence interval (CI): 2.84, 3.85) and after PSM (HR: 1.62; 95%CI: 1.31, 2.00). The modified TNM staging, equating one TD to four LNMs, achieved superior prognostic performance, surpassing the 8th edition AJCC TNM staging and other modified systems (C-index: 0.751, AIC: 15954.0). In this system, 12.04% (26/216) of TD-positive patients were upstaged from stage II to stage III. These upstaged patients had worse outcomes than the remaining stage II patients (HR: 10.97; 95% CI: 4.55-26.44), while outcomes were similar to those of original stage III patients (HR:1.08; 95%CI: 0.66, 1.78).</p><p><strong>Conclusion: </strong>The presence and increased number of TDs were noted to be associated with GC patients' poor prognosis. Integrating TD count with LNMs could enhance the prognostic accuracy of the TNM staging system.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"761-773"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143439950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Construction and validation of a regulatory T cells-based classification of renal cell carcinoma: an integrated bioinformatic analysis and clinical cohort study.","authors":"Yuntao Yao, Yifan Liu, Bingnan Lu, Guo Ji, Lei Wang, Keqin Dong, Zihui Zhao, Donghao Lyu, Maodong Wei, Siqi Tu, Xukun Lyu, Yuanan Li, Runzhi Huang, Wang Zhou, Guofeng Xu, Xiuwu Pan, Xingang Cui","doi":"10.1007/s13402-024-01030-9","DOIUrl":"10.1007/s13402-024-01030-9","url":null,"abstract":"<p><strong>Purpose: </strong>Renal cell carcinoma (RCC), exhibiting remarkable heterogeneity, can be highly infiltrated by regulatory T cells (Tregs). However, the relationship between Treg and the heterogeneity of RCC remains to be explored.</p><p><strong>Methods: </strong>We acquired single-cell RNA-seq profiles and 537 bulk RNA-seq profiles of TCGA-KIRC cohort. Through clustering, monocle2 pseudotime and prognostic analyses, we identified Treg states-related prognostic genes (TSRPGs), then constructing the RCC Treg states-related prognostic classification (RCC-TSC). We also explored its prognostic significance and multi-omics landmarks. Additionally, we utilized correlation analysis to establish regulatory networks, and predicted candidate inhibitors. More importantly, in Xinhua cohort of 370 patients with kidney neoplasm, we used immunohistochemical (IHC) staining for classification, then employing statistical analyses including Chi-square tests and multivariate Cox proportional hazards regression analysis to explore its clinical relevance.</p><p><strong>Results: </strong>We defined 44 TSRPGs in four different monocle states, and identified high immune infiltration RCC (HIRC, LAG3+, Mki67+) as the highly exhausted subtype with the worst prognosis in RCC-TSC (p < 0.001). BATF-LAG3-immune cells axis might be its underlying metastasis-related mechanism. Immunotherapy and inhibitors including sunitinib potentially conferred best therapeutic effects for HIRC. Furthermore, we successfully validated HIRC subtype as an independent prognostic factor within the Xinhua cohort (OS, HR = 16.68, 95% CI = 1.88-148.1, p = 0.011; PFS, HR = 4.43, 95% CI = 1.55-12.6, p = 0.005).</p><p><strong>Conclusion: </strong>Through integrated bioinformatics analysis and a large-sample retrospective clinical study, we successfully established RCC-TSC and a diagnostic kit, which could stratify RCC patients with different prognosis and to guide personalized treatment.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"591-615"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Three-dimensional genome architecture in intrahepatic cholangiocarcinoma.","authors":"Youfeng Liang, Cong Li, Renchao Zou, Lu Ying, Xiaoyang Chen, Zhaohai Wang, Wenjing Zhang, Mingxuan Hao, Hao Yang, Rui Guo, Guanglin Lei, Fang Sun, Kexu Zhao, Yu Zhang, Jia Dai, Shangya Feng, Keyue Zhang, Luyuan Guo, Shuyue Liu, Chuanxing Wan, Lin Wang, Penghui Yang, Zhao Yang","doi":"10.1007/s13402-024-01033-6","DOIUrl":"10.1007/s13402-024-01033-6","url":null,"abstract":"<p><strong>Purpose: </strong>Intrahepatic cholangiocarcinoma (ICC) is a common primary hepatic tumors with a 5-year survival rate of less than 20%. Therefore, it is crucial to elucidate the molecular mechanisms of ICC. Recently, the advance of high-throughput chromosome conformation capture (Hi-C) technology help us look insight into the three-dimensional (3D) genome structure variation during tumorigenesis. However, its function in ICC pathogenesis remained unclear.</p><p><strong>Methods: </strong>Hi-C and RNA-sequencing were applied to analyze 3D genome structures and gene expression in ICC and adjacent noncancerous hepatic tissue (ANHT). Furthermore, the dysregulated genes due to 3D genome changes were validated via quantitative real-time PCR and immunohistochemistry.</p><p><strong>Results: </strong>Primarily, the intrachromosomal interactions of chr1, chr2, chr3, and chr11 and the interchromosomal interactions of chr1-chr10, chr13-chr21, chr16-chr19, and chr19-chr22 were also significantly distinct between ANHT and ICC, which may potentially contribute to the activation of cell migration and invasion via the upregulation of WNT10A, EpCAM, S100A3/A6, and MAPK12. Interestingly, 56 compartment regions from 23 chromosomes underwent A to B or B to A transitions during ICC oncogenesis, which attenuated the complement pathway through the downregulation of C8A/C8B, F7, F10, and F13B. Notably, topologically associated domain (TAD) rearrangements were identified in the region containing HOPX (chr4: 57,514,154-57,522,688) and ACVR1 (chr2:158,592,958-158,732,374) in ICC, which may contribute to the hijacking of remote enhancers that were previously outside the TAD and increased expression of HOPX and ACVR1.</p><p><strong>Conclusions: </strong>This study reveals relationship between 3D genome structural variations and gene dysregulation during ICC tumorigenesis, indicating the molecular mechanisms and potential biomarkers.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"617-635"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Publisher Correction to: LPA released from dying cancer cells after chemotherapy inactivates Hippo signaling and promotes pancreatic cancer cell repopulation.","authors":"Yuzhi Liu, Jie Ding, Shumin Li, Anyi Jiang, Zhiqin Chen, Ming Quan","doi":"10.1007/s13402-025-01047-8","DOIUrl":"10.1007/s13402-025-01047-8","url":null,"abstract":"","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"673"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143439953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UBE2Q2 promotes tumor progression and glycolysis of hepatocellular carcinoma through NF-κB/HIF1α signal pathway.","authors":"Xiaoling Wu, Yiran Chen, Wenzhi He, Ye Yao, Yingyi Liu, Peng Xia, Hao Zhang, Xiaomian Li, Yonghua Guo, Xi Chen, Weijie Ma, Yufeng Yuan","doi":"10.1007/s13402-025-01037-w","DOIUrl":"10.1007/s13402-025-01037-w","url":null,"abstract":"<p><strong>Purpose: </strong>Metabolic reprogramming, particularly the Warburg effect, plays a crucial role in the onset and progression of tumors. The ubiquitin-conjugating enzyme E2 Q2 (UBE2Q2) has been identified overexpressed in hepatocellular carcinoma (HCC). Our aim was to determine if UBE2Q2 plays a role in regulating glycolysis, contributing to the carcinogenesis of HCC.</p><p><strong>Methods: </strong>Bioinformatics analysis, western blot and qPCR were used to detect the expression of UBE2Q2. Functional experiments, proteomics analysis and subcutaneous tumors were constructed to find the biological function of UBE2Q2 in HCC. Co-immunoprecipitation, western blot and ubiquitination assays were used to identify the mechanisms involved.</p><p><strong>Results: </strong>We found a significant association between high UBE2Q2 expression and poor prognosis in HCC patients. Functionally, UBE2Q2 was shown to advance tumor progression in HCC through both in vitro assays and in vivo assessments. Proteomics analysis and glycolysis stress tests corroborated an increase in glycolytic activity due to UBE2Q2. Our findings reveal that UBE2Q2 augments glycolysis by boosting the transcription levels of hypoxia-inducible factor 1α (HIF1α), primarily through the activation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. At the molecular level, UBE2Q2 interaction with baculoviral IAP repeat-containing 2 (cIAP1) orchestrates the K63-linked ubiquitination of receptor-interacting serine/threonine-protein kinase 1 (RIP1), which in turn, activates the NF-κB signaling pathway.</p><p><strong>Conclusions: </strong>Our investigation reveals that UBE2Q2 regulates the glycolysis in HCC through modulation of the NF-κB/HIF1α signaling pathway, pinpointing UBE2Q2 as a promising therapeutic target for the disease.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"637-654"},"PeriodicalIF":6.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}