Oncologie最新文献

{"title":"CAP1 signaling regulates tumor immunity, proliferation, and migration in esophageal cancer","authors":"Xu Li, Jinming Tang, Kele Qin, Xun Wu, Jiahui Wu, Xiaolong Sheng","doi":"10.1515/oncologie-2025-0172","DOIUrl":"https://doi.org/10.1515/oncologie-2025-0172","url":null,"abstract":"Abstract Objectives Esophageal cancer (ESCA) is a common malignancy with high morbidity and mortality. Our study aimed to explore the regulatory pathways of CAP1 in ESCA and its effects on tumor immunity. Methods Immune-related differentially expressed genes (DEGs) associated with ESCA prognosis were screened through bioinformatics analysis, and a risk prognosis model was constructed. In addition, we employed a combination of in vitro techniques, including qRT-PCR, Western blot, CCK-8, Transwell, co-culture, CHIP, and dual-luciferase reporter assays, to systematically investigate the expression, function, and transcriptional regulation of CAP1 in ESCA. Furthermore, the role of the ELF1/CAP1 axis was verified using a xenograft tumor model. Results Bioinformatics analysis using LASSO Cox regression demonstrated that CAP1 carried the highest risk coefficient (0.4437) in the prognostic model. The risk score model demonstrated excellent predictive performance in the TCGA cohort and was successfully validated in external GEO datasets. High expression of CAP1 in ESCA cells enhanced their proliferative, migratory, and invasive capabilities (p<0.001). In a co-culture system, silencing CAP1 in ESCA cells enhanced the cytotoxicity of CD8+ T cells and reduced their apoptosis (p<0.001). The transcription factor ELF1 promoted CAP1 expression by binding to its promoter, thereby regulating immune evasion and tumor progression in ESCA. Importantly, in vivo experiments confirmed that knockdown of either ELF1 or CAP1 significantly suppressed tumor growth, enhanced CD8+ T cell infiltration, and downregulated PD-L1 expression (p<0.001), demonstrating that ELF1 promotes tumor progression and immune escape in ESCA via CAP1. Conclusion CAP1 promotes ESCA progression by regulating tumor immunity, cell proliferation, and migration. ELF1 plays a crucial role in ESCA by transcriptionally regulating CAP1 expression. These findings identify the ELF1/CAP1 axis as a promising therapeutic target and prognostic biomarker for ESCC.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":"28 2","pages":"379-395"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/oncologie-2025-0172/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147900906","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":"PCDH8 promotes malignant progression of cervical cancer via the Wnt/β-catenin axis","authors":"Meisongzhu Yang, Jiapei Peng, Hui Li","doi":"10.1515/oncologie-2025-0194","DOIUrl":"https://doi.org/10.1515/oncologie-2025-0194","url":null,"abstract":"Abstract Objectives Dysregulated expression of protocadherin 8 (PCDH8) has been observed in several malignancies and is associated with cancer progression. Yet, its role in cervical carcinogenesis requires systematic investigation. This investigation seeks to elucidate the molecular mechanisms of PCDH8-mediated malignant phenotypic regulation in cervical cancer, thereby identifying novel biomarkers for early diagnosis and providing a foundation for the development of targeted therapies. Methods Metastasis-associated genes were determined by differential expression analysis on the Cancer Genome Atlas (TCGA) cervical cancer database. PCDH8 overexpression models were established in SiHa cells, and knockdown models were established in HeLa cells. Transfection efficiency and molecular mechanisms were assessed. Cell functions were evaluated. Gene Set Enrichment Analysis (GSEA) identified PCDH8-related signaling pathways. TOP/FOP dual-luciferase reporter system quantified pathway activity. β-catenin functional intervention experiments validated PCDH8-mediated regulatory mechanisms. Results Cervical cancer datasets from TCGA revealed significant PCDH8 upregulation in metastatic (n=68) vs. the non-metastatic (n=79). High PCDH8 expression was linked to reduced median overall survival (n=55; p=0.024) and metastasis-free survival (n=55; p=0.006). PCDH8 overexpression enhanced the proliferative, migratory, and invasive capacities of cervical cancer cells; in contrast, PCDH8 knockdown attenuated these outcomes. Mechanistically, PCDH8 stimulated the Wnt/β-catenin pathway, upregulating metalloproteinase-7 (MMP7), Cyclin D1, and c-Myc to drive malignant phenotypes of cervical cancer cells. However, β-catenin knockdown reversed these effects. Conclusions PCDH8 drives the malignant phenotypes of cervical cancer cells via activating the Wnt/β-catenin pathway. This study identifies a potential therapeutic target and suggests potential clinical implications for improving cervical cancer patient prognosis.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":"28 1","pages":"199-210"},"PeriodicalIF":0.0,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/oncologie-2025-0194/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147899399","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":"VTA1 and breast cancer: a potential indicator for diagnostic and prognostic evaluation","authors":"Yongfeng Wang, Xinyue Yang, Xianglai Jiang, Jiayang Guo, Hao Yang, Siyang Yin, Zechen Zhang, Donghai Li, Sheng Li","doi":"10.1515/oncologie-2025-0253","DOIUrl":"https://doi.org/10.1515/oncologie-2025-0253","url":null,"abstract":"Abstract Objectives Vacuolar protein sorting-associated protein VTA1 homolog (VTA1) encodes a factor involved in multivesicular body trafficking. This investigation sought to determine if VTA1 might function as a diagnostic indicator, a standalone prognostic element, and a potential therapeutic target in breast cancer. Methods We performed a pan-cancer analysis of VTA1 expression using TCGA data from 33 cancer types and assessed immune infiltration with TIMER2.0. Breast cancer data from TCGA and Gene Expression Omnibus (GEO) database were collected to complete the difference analysis, clinical feature correlation, prognosis analysis, enrichment analysis, and tumor microenvironment score analysis of VTA1 in BRCA. The presence of VTA1 in BRCA cells was verified by Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR), Western Blot (WB), and Immunohistochemistry (IHC). Results VTA1 expression was markedly elevated in breast cancer. Elevated levels were significantly linked to worse overall survival (OS). (hazard ratio [HR] = 1.791, 95 % CI: 1.206–2.659, p<0.01) and recurrence-free survival (RFS), indicating that VTA1 is an independent prognostic factor. In the tumor immune microenvironment, high VTA1 expression correlated with increased infiltration of myeloid and resting immune cells but decreased effector/activated immune cells, suggesting poor prognosis. Conclusions VTA1 is a promising prognostic indicator for various cancers, particularly in breast cancer. The expression of VTA1 is markedly elevated in breast cancer tissues relative to the adjacent normal tissues. Clinical analyses further suggest that VTA1 functions as an independent indicator associated with unfavorable outcomes in breast cancer. These findings imply that VTA1 may serve as a promising biomarker for diagnosis, therapeutic guidance, and survival prediction.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":"27 6","pages":"1007-1028"},"PeriodicalIF":0.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147890400","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 ENST00000539930 transcript predicts sensitivity to PARP inhibitors and clinical prognosis in cancers","authors":"Chi Xu, Cong Li, Wenna Wang, Yiqun Li, Ting Wang, Fangzhou Sun, Xiaoqi Yang, Chunxiao Li, Fei Ma","doi":"10.1515/oncologie-2025-0144","DOIUrl":"https://doi.org/10.1515/oncologie-2025-0144","url":null,"abstract":"Abstract Objectives Synthetic lethality-based cancer therapy, particularly using PARP inhibitors, faces resistance challenges. This study aims to explore the role of gene-specific transcripts due to alternative splicing in PARP inhibitor resistance. Methods This study conducted transcript-level correlation analyses using CCLE and GDSC databases to identify associations between PARP2 splice variants and sensitivity to PARP inhibitors. This study validated the findings through in vitro overexpression experiments in MDA-MB-231 breast cancer cells and organoid models derived from ovarian cancer patients. Cytotoxicity assays were performed to assess olaparib sensitivity, and RNA sequencing was applied to examine transcriptomic changes. Functional enrichment analyses and clinical prognosis evaluations were conducted using TCGA datasets. Results The PARP2 splice variant ENST00000539930 showed a strong correlation with PARP inhibitors sensitivity, outperforming total PARP2 gene expression. Overexpression of ENST00000539930 in MDA-MB-231 cells significantly increased sensitivity to olaparib. Patient-derived ovarian cancer organoids confirmed this correlation (r=−0.43, p=0.04). Transcriptomic analysis revealed that ENST00000539930 expression was associated with activation of RNA splicing and inhibition of DNA repair pathways. Clinically, high ENST00000539930 expression predicted improved survival in breast, ovarian, and pancreatic cancer cohorts (HR=0.62–0.71, p<0.05). Conclusions ENST00000539930 is a splice variant of PARP2 that predicts enhanced sensitivity to PARP inhibitors and favorable clinical outcomes. This study highlights the potential of transcript-specific biomarkers and the importance of alternative splicing in cancer therapy response.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":"27 6","pages":"991-1005"},"PeriodicalIF":0.0,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/oncologie-2025-0144/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147906108","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":"Development of an adenosine-related RiskScore model to predict the prognosis of patients with ovarian cancer","authors":"Cheng Peng, Yuan Zhang, Lilin Liu, Huanhuan Li","doi":"10.1515/oncologie-2025-0104","DOIUrl":"https://doi.org/10.1515/oncologie-2025-0104","url":null,"abstract":"Abstract Objectives This study aims to explore the crucial functions of adenosine-related genes (ARGs) in immune activity and the development of ovarian cancer (OC). Methods Adenosine score was calculated by “GSVA” package. Key module genes were identified by weighted correlation network analysis (WGCNA). Least absolute shrinkage and selection operator (LASSO) Cox regression analysis was performed to select ARGs, which were combined to develop a RiskScore model. Gene set enrichment analysis (GSEA) was conducted for functional enrichment analysis, and immune infiltration in different risk groups was assessed. Somatic mutation was analyzed by MuTect2 and visualized by “maftools” package. The viability, migration, and invasion of two OC cell lines (A2780 and SK-OV-3) were measured by cell counting kit-8 (CCK-8), wound healing, and Transwell assays. Results To accurately predict the prognosis of OC, 9 ARGs ( PIK3CG , VSIG4 , MATK , PIEZO1 , RARRES1 , SELL , S1PR4 , IL18BP and CD40LG ) were identified to construct a RiskScore model. Functional enrichment analysis revealed that immunity-correlated pathways were predominantly enriched in the low-risk group, whereas inflammation-associated pathways were significantly enriched in the high-risk group. In vitro assays revealed a high expression of most of the 9 ARGs in OC cells, except MATK and SELL . Notably, silencing VSIG4 markedly suppressed the proliferation, migration, and invasion of the OC cells. Conclusions This study not only provides novel insights into the prognosis evaluation of patients with OC but also offers possibilities for formulating targeted therapeutic strategies and personalized treatment plans.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/oncologie-2025-0104/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147905006","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":"Propofol anesthesia for gastric cancer surgery increased cancer suppressor miR-122-5p expression in plasma extracellular vesicles compared with sevoflurane","authors":"Mohan Tian, Pengbo Zhang, Miao Miao, Kaijiong Hou, Xiaolin Sun, Xiaotong Li, Zhuo Chen, Shan Yu, Hong Chen","doi":"10.1515/oncologie-2025-0184","DOIUrl":"https://doi.org/10.1515/oncologie-2025-0184","url":null,"abstract":"Abstract Objectives The impact of anesthetic drugs on cancer cells is controversial. As propofol and sevoflurane are widely used in gastric cancer surgery, this study aimed to investigate their effects on microRNA (miRNA) expression in plasma extracellular vesicles (EVs) and on circulating gastric cancer cells during surgery. Methods We collected the plasma of 10 patients with gastric adenocarcinoma who were anesthetized with propofol or sevoflurane for sequencing. Differentially expressed miRNAs were screened via DESeq2 and verified by qPCR in another 18 paired samples from nine patients before and after propofol anesthesia. Plasma EVs were stained with PKH26 and cocultured with GES-1 and AGS cells, and miR-122-5p expression was determined. The target genes were analyzed using MiRanda/RNAhybrid/KEGG/KM plotter. Results 19 (13 upregulated/6 downregulated) and 5 (2 upregulated/3 downregulated) differentially expressed miRNAs were identified after propofol and sevoflurane, respectively. MAPK, AKT1, AKT2, and EGFR were the target genes of the propofol-upregulated miRNAs. miR-122-5p expression in the plasma EVs of patients after propofol increased by an average of 6.2-fold (p=0.011). After coculture, hsa-miR-122-5p expression was significantly greater in both the GES-1 and AGS cell lines than in the control group. High expression of the hsa-miR-122-5p target gene PPP2R2D was significantly correlated with reduced overall survival (hazard ratio [HR] = 1.56, p=5.5 × 10 −5 ), whereas high expression of PPP2R5B predicted poorer survival (HR=1.41, p=6.7 × 10 −5 ). Conclusions miR-122-5p in plasma EVs was affected by propofol and serves as an inhibitor of gastric cancer.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":"27 5","pages":"825-838"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/oncologie-2025-0184/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147900926","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":"Artesunate overcomes icotinib resistance in non-small cell lung cancer with <i>EGFR</i>-sensitive mutations","authors":"Tongwei Zhao, Zheling Chen, Jianbin Zhang, Guoqing Ru, Hangjie Ying, Xin Zhang, Ming Chen","doi":"10.1515/oncologie-2025-0161","DOIUrl":"https://doi.org/10.1515/oncologie-2025-0161","url":null,"abstract":"Abstract Objectives Due to increasing severity of resistance to first-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in EGFR -mutant non-small cell lung cancer (NSCLC) patients, this study investigated whether artesunate overcomes such resistance specifically to icotinib hydrochloride (icotinib) and explored its mechanisms. Methods We evaluated anti-tumor effects of artesunate in icotinib- and cross-resistant NSCLC models (NCI-H1975, PC-9/GR cells, and NCI-H1975 xenografts). Effects of GAB1 knockdown/overexpression and artesunate on EGFR–Gab1–SHP2–ERK and EGFR–PI3K pathways were analyzed. Clinical correlations between Gab1 and phosphorylated Gab1 (pGab1) expressions and outcomes were analyzed in specimens. Results Artesunate significantly inhibited proliferation and induced apoptosis in resistant EGFR -mutant/T790M+ models. Gab1 overexpression characterized icotinib-resistant cells. GAB1 knockdown suppressed SHP2/phosphorylated ERK (pERK) expression, reducing proliferation and promoting apoptosis. Rescue experiments confirmed that GAB1 overexpression promoted proliferation and suppressed apoptosis via ERK activation. Artesunate downregulated phosphorylated EGFR (pEGFR), pGab1, SHP2, pERK1/2, and total EGFR/Gab1. Downregulated pGab1 was correlated with improved efficacy of first-line EGFR-TKIs and patient prognosis. Patients with low pGab1 expression exhibited significantly prolonged median progression-free survival (PFS; 17.3 vs. 8.8 months, HR=0.345, p&lt;0.001) and a significantly elevated objective response rate (ORR; 83.9 % vs. 31.0 %, p&lt;0.001) compared to those with high pGab1 expression. Conclusions Artesunate overcomes icotinib resistance in NSCLC through suppression of proliferation and activation of apoptosis via the EGFR–Gab1–SHP2–ERK axis. Gab1 regulates resistance via SHP2–ERK, highlighting its therapeutic potential. These findings support artesunate as a clinically translatable agent for overcoming resistance of first-generation EGFR-TKIs.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":"27 5","pages":"807-824"},"PeriodicalIF":0.0,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/oncologie-2025-0161/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147915931","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":"Integrated RNA sequencing reveals tumor microenvironment heterogeneity and immunosuppressive role of M2 macrophages in osteosarcoma","authors":"Zhijun Ding, Yi Li, Cheng Zhong","doi":"10.1515/oncologie-2025-0225","DOIUrl":"https://doi.org/10.1515/oncologie-2025-0225","url":null,"abstract":"Abstract Objectives Osteosarcoma, a prevalent malignant bone tumor in pediatric and adolescent populations, is characterized by a markedly diverse tumor microenvironment (TME) that complicates therapeutic intervention. Among the key components of the TME, M2 macrophages contribute to immune suppression, tumor progression, and resistance to therapy. This study aims to explore the immune microenvironment of osteosarcoma and identify key immunosuppressive components using integrated transcriptomic analysis. Methods We integrated scRNA-seq (GSE152048) and bulk RNA-seq (TARGET) data to characterize the osteosarcoma tumor microenvironment. Key analyses included cell clustering and annotation (Seurat), pseudotime trajectory (Monocle 2), cell-cell communication (CellChat), and M2 macrophage deconvolution (CIBERSORT, BayesPrism). Gene modules were identified via WGCNA, and drug sensitivity was predicted using oncoPredict. Key genes were validated by qRT-PCR and Western blot. Results Our integrated analysis revealed that M2 macrophage infiltration was significantly associated with an immunosuppressive tumor microenvironment in osteosarcoma. Weighted gene co-expression network analysis (WGCNA) identified gene modules highly correlated with M2 macrophage abundance and immune evasion signatures. Reduced M2 infiltration was linked to altered transcriptional patterns and increased predicted sensitivity to Etoposide and Doxorubicin. Two immune-related genes, PTK2B and PTPRC, were significantly upregulated in osteosarcoma samples and validated by RT-qPCR and Western blotting in U2OS cells. Conclusions This study demonstrates that M2 macrophage infiltration is a defining feature of the osteosarcoma immune microenvironment and is associated with immune suppression. Through integrative transcriptomic analysis, PTK2B and PTPRC were identified as key immune-related genes linked to M2 macrophage abundance and patient prognosis. These results establish a transcriptional basis for the immunosuppressive phenotype in osteosarcoma.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":"27 5","pages":"759-778"},"PeriodicalIF":0.0,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/oncologie-2025-0225/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147900279","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":"Integrative analyses identify the mechanism by which HSPA9 influences glioma energy metabolism","authors":"Wenying He, Qinghua Zhang, Jixin Xie, Fang Wu, Lijuan Wang, Libin Wang","doi":"10.1515/oncologie-2025-0097","DOIUrl":"https://doi.org/10.1515/oncologie-2025-0097","url":null,"abstract":"Abstract Objectives Heat shock protein family A (Hsp70) member 9 (HSPA9) is a mitochondrial chaperone protein that belongs to the heat shock protein 70 family. HSPA9 is expressed across various malignancies. However, the intricate relationship and mechanisms between HSPA9 and glioma remain unclear. This study aims to elucidate the molecular mechanisms by which HSPA9 influences glioma progression through transcriptomic and proteomic analysis. Methods HSPA9 expression in glioma patient tissues was validated by histopathological analysis and Western blotting. Subsequently, stable HSPA9-overexpressing and HSPA9-knockdown U-87 MG and U251 MG cell lines were generated. To investigate the downstream effects, transcriptomic and proteomic sequencing was performed on HSPA9-knockdown U-87 MG cells. Bioinformatics analysis was then applied to identify enriched pathways associated with the differentially expressed genes and proteins. Finally, key metabolites related to these pathways were quantified. Results Immunohistochemistry and Western blotting revealed a significant elevation of HSPA9 expression in glioma tissues, indicating its potential as a molecular marker for this malignancy. Integrated transcriptomic-proteomic analysis detected 496 downregulated genes and 276 upregulated proteins in HSPA9-knockdown U-87 MG cells. Pathway enrichment analysis indicated that these differentially expressed molecules were primarily enriched in energy metabolism-related pathways. Metabolic assays using commercial kits demonstrated that knockdown of HSPA9 reduced lactate levels in both U-87 MG and U251 MG cells, accompanied by increased glucose and ATP levels. Conversely, in HSPA9-overexpressing U-87 MG and U251 MG cell lines, α-ketoglutarate (α-KG) levels were consistently decreased. Conclusion The results demonstrated that HSPA9 could drive glioma cells from oxidative phosphorylation toward glycolytic metabolism, thereby accelerating tumor cell proliferation. This study provides novel insights into the influence of HSPA9 on the initiation and progression of glioma through gene and protein expression. Further research needs to be conducted to investigate the potential therapeutic target of HSPA9 in glioma.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":"27 4","pages":"545-561"},"PeriodicalIF":0.0,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/oncologie-2025-0097/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147331270","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":"Establishment of whole tumor cell antigen-induced cellular immunotherapy for lung adenocarcinoma","authors":"Binghan Zhu, Xiaoping Qian, Kaiyuan Zhang, Yali Peng, Biao Liu, Guichun Huang, Yan Li","doi":"10.1515/oncologie-2025-0137","DOIUrl":"https://doi.org/10.1515/oncologie-2025-0137","url":null,"abstract":"Abstract Objectives Although immunotherapy improves the prognosis of many current advanced malignancies, many patients still do not respond or develop resistance after immunotherapy. The key point of cancer immunotherapy is whether the immune system can recognize the tumor as a foreign body. However, lung adenocarcinoma (LUAD) is a tumor with weak immunogenicity, and many patients do not benefit from immunotherapy. This study aimed to optimize the adoptive cell immunotherapy process and propose a new pipeline for LUAD immunotherapy. Methods This study optimized the process of adoptive cell immunotherapy by adding individualized and enhanced whole tumor cell antigens (WTCAs) modified by chemotherapeutics, irradiation, or freezing. Venous blood from lung adenocarcinoma patients was collected to extract peripheral blood mononuclear cells (PBMCs). This study also verified the efficacy of the new strategy for LUAD immunotherapy by Flow Cytometry analysis, EdU proliferation assay, Annexin V-FITC/PI apoptosis assay, and Animal models in vivo and in vitro , etc. Results WTCAs could enhance the proliferation of immune-effective CD8 + cells and inhibit the apoptosis of immune-effective CD8 + cells, especially for X-ray-induced WTCA. The efficacy of WTCAs-induced cell immunotherapy for LUAD in vitro and vivo was prominent. Tumor size was significantly reduced by adoptive cell immunotherapy, whether specific or non-specific. In contrast, WTCAs-induced immune cells induced by 4 Gy X-ray irradiation or high-dose cisplatin (10 μg/mL) had a more effective tumor inhibition capability than all other groups (p&lt;0.001). Conclusion The adoptive tumor-specific immune cells activated by X-ray-induced WTCA could elicit the most effective tumor inhibition. This study provides new ideas for future individualized cell immunotherapy of LUAD.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":"27 4","pages":"575-588"},"PeriodicalIF":0.0,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/oncologie-2025-0137/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147914564","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}