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Addendum: Assessment of cholecystokinin 2 receptor (CCK2R) in neoplastic tissue. 附录:肿瘤组织中胆囊收缩素2受体(CCK2R)的评估。
Oncotarget Pub Date : 2025-03-06 DOI: 10.18632/oncotarget.28699
Jyoti Roy, Karson S Putt, Domenico Coppola, Marino E Leon, Farah K Khalil, Barbara A Centeno, Noel Clark, Valerie E Stark, David L Morse, Philip S Low
{"title":"Addendum: Assessment of cholecystokinin 2 receptor (CCK2R) in neoplastic tissue.","authors":"Jyoti Roy, Karson S Putt, Domenico Coppola, Marino E Leon, Farah K Khalil, Barbara A Centeno, Noel Clark, Valerie E Stark, David L Morse, Philip S Low","doi":"10.18632/oncotarget.28699","DOIUrl":"10.18632/oncotarget.28699","url":null,"abstract":"","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"132"},"PeriodicalIF":0.0,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retraction: FKBP14 overexpression contributes to osteosarcoma carcinogenesis and indicates poor survival outcome. 撤回:FKBP14过表达有助于骨肉瘤的癌变,并预示较差的生存结果。
Oncotarget Pub Date : 2025-02-28 DOI: 10.18632/oncotarget.28697
Zhongming Huang, Junhua Li, Shaohua Du, Yanghua Tang, Ligang Huang, Luwei Xiao, Peijian Tong
{"title":"Retraction: FKBP14 overexpression contributes to osteosarcoma carcinogenesis and indicates poor survival outcome.","authors":"Zhongming Huang, Junhua Li, Shaohua Du, Yanghua Tang, Ligang Huang, Luwei Xiao, Peijian Tong","doi":"10.18632/oncotarget.28697","DOIUrl":"10.18632/oncotarget.28697","url":null,"abstract":"","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"131"},"PeriodicalIF":0.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11870124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143524057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effect of TIMPs and their minimally engineered variants in blocking invasion and migration of brain cancer cells. TIMPs及其最小工程化变体在阻断脑癌细胞侵袭和迁移中的作用。
Oncotarget Pub Date : 2025-02-28 DOI: 10.18632/oncotarget.28691
Elham Taheri, Maryam Raeeszadeh-Sarmazdeh
{"title":"Effect of TIMPs and their minimally engineered variants in blocking invasion and migration of brain cancer cells.","authors":"Elham Taheri, Maryam Raeeszadeh-Sarmazdeh","doi":"10.18632/oncotarget.28691","DOIUrl":"10.18632/oncotarget.28691","url":null,"abstract":"<p><p>Matrix metalloproteinases (MMPs) are crucial in remodeling the extracellular matrix (ECM), modulating key processes involved in cancer progression, such as migration, invasion, angiogenesis, and metastasis. The overexpression of MMPs, particularly MMP-9, is markedly observed in glioblastoma multiforme (GBM), an aggressive primary brain tumor known for its diffuse and infiltrative nature. Tissue inhibitors of metalloproteinases (TIMPs), endogenous MMP inhibitors, offer significant therapeutic potential due to their wider interaction interfaces relative to small molecule inhibitors. Here, we studied the effect of wild-type human TIMP-1 and TIMP-3 and minimal TIMP variants (mTC1 and mTC3), previously engineered for MMP inhibition, on migration and invasion of GBM cells. Our study focused on minimal TIMP variants, due to their small molecular size and potential in higher cellular uptake and delivery, to assess their potential in cell-based assays. The results demonstrated that the minimal TIMP variants, mTC1, and mTC3, effectively inhibit MMP activity underscoring their potential to limit tumor invasion and progression. Given the lethal nature of GBM and the limited efficacy of current therapies, the application of TIMPs and their engineered minimal variants represents a novel and potentially transformative approach to regulating MMP activity in GBM.</p>","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"118-130"},"PeriodicalIF":0.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11870142/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143524056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retraction: Ftx non coding RNA-derived miR-545 promotes cell proliferation by targeting RIG-I in hepatocellular carcinoma. 撤回:Ftx非编码rna衍生的miR-545通过靶向肝细胞癌中的RIG-I促进细胞增殖。
Oncotarget Pub Date : 2025-02-18 DOI: 10.18632/oncotarget.28695
Zhikui Liu, Changwei Dou, Bowen Yao, Meng Xu, Linglong Ding, Yufeng Wang, Yuli Jia, Qing Li, Hongyong Zhang, Kangsheng Tu, Tao Song, Qingguang Liu
{"title":"Retraction: Ftx non coding RNA-derived miR-545 promotes cell proliferation by targeting RIG-I in hepatocellular carcinoma.","authors":"Zhikui Liu, Changwei Dou, Bowen Yao, Meng Xu, Linglong Ding, Yufeng Wang, Yuli Jia, Qing Li, Hongyong Zhang, Kangsheng Tu, Tao Song, Qingguang Liu","doi":"10.18632/oncotarget.28695","DOIUrl":"10.18632/oncotarget.28695","url":null,"abstract":"","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"102"},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143449670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Leukopenia, weight loss and oral mucositis induced by 5-Fluorouracil in hamsters' model: A regenerative approach using electrospun poly(Lactic-co-Glycolic Acid) membrane. 5-氟尿嘧啶致仓鼠白细胞减少、体重减轻和口腔黏膜炎模型:静电纺丝聚乳酸-羟基乙酸膜再生方法
Oncotarget Pub Date : 2025-02-18 DOI: 10.18632/oncotarget.28685
Ana Chor, Hélio Dos Santos Dutra, Marcos Lopes Dias, Raquel Pires Gonçalves, Christina Maeda Takiya, Alexandre Malta Rossi, Marcos Farina
{"title":"Leukopenia, weight loss and oral mucositis induced by 5-Fluorouracil in hamsters' model: A regenerative approach using electrospun poly(Lactic-co-Glycolic Acid) membrane.","authors":"Ana Chor, Hélio Dos Santos Dutra, Marcos Lopes Dias, Raquel Pires Gonçalves, Christina Maeda Takiya, Alexandre Malta Rossi, Marcos Farina","doi":"10.18632/oncotarget.28685","DOIUrl":"10.18632/oncotarget.28685","url":null,"abstract":"<p><p>Clinical parameters of leukogram and weight were analyzed in animal models before and after seven days of 5-FU infusions. A comparison of leukograms before and after 5-FU administrations was analyzed. The results showed a significant difference (<i>p</i> = 0,004), confirming immunosuppression. There was a decrease in the weight of the animals after 7 days of 5-FU infusions (<i>p</i> = 0.02). After immunosuppression occurred, oral mucositis (OM) ulcerative lesions were observed. Two of the animals were selected to receive PLGA dressings. Then, electrospun PLGA membranes, with or without autologous cells, were applied to the ulcerative lesions, aiming to accelerate the regeneration process. Although this therapeutic innovation for OM lesions was still not tested in the bioengineering area, morphological analysis presented promising results. Lesions covered by cell-free PLGA, exhibited areas of inflammation persistence and angiogenesis. The cell-seeded cell-seeded PLGA membrane exhibited complete reepithelialization after 6 days, with minor inflammatory infiltrate. Interestingly, the present work showed preclinical parameters of cachexia induced by chemotherapy for cancer treatment. Moreover, it showed an innovative approach by applying dressings consisting of electrospun PLGA with the addition of autologous mesenchymal cells for OM ulcerative lesions. This promising innovation will pave the way for future applications in oral mucosa lesions.</p>","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"103-117"},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143449668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retraction: Methylation-mediated repression of microRNA-129-2 suppresses cell aggressiveness by inhibiting high mobility group box 1 in human hepatocellular carcinoma. 回顾:甲基化介导的抑制microRNA-129-2通过抑制人肝细胞癌的高迁移率组盒1来抑制细胞侵袭性。
Oncotarget Pub Date : 2025-02-18 DOI: 10.18632/oncotarget.28694
Zhikui Liu, Changwei Dou, Bowen Yao, Meng Xu, Linglong Ding, Yufeng Wang, Yuli Jia, Qing Li, Hongyong Zhang, Kangsheng Tu, Tao Song, Qingguang Liu
{"title":"Retraction: Methylation-mediated repression of microRNA-129-2 suppresses cell aggressiveness by inhibiting high mobility group box 1 in human hepatocellular carcinoma.","authors":"Zhikui Liu, Changwei Dou, Bowen Yao, Meng Xu, Linglong Ding, Yufeng Wang, Yuli Jia, Qing Li, Hongyong Zhang, Kangsheng Tu, Tao Song, Qingguang Liu","doi":"10.18632/oncotarget.28694","DOIUrl":"10.18632/oncotarget.28694","url":null,"abstract":"","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"101"},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143449672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Robust p53 phenotypes and prospective downstream targets in telomerase-immortalized human cells. 端粒酶永生化人类细胞中强健的p53表型和预期的下游靶点。
Oncotarget Pub Date : 2025-02-18 DOI: 10.18632/oncotarget.28690
Jessica J Miciak, Lucy Petrova, Rhythm Sajwan, Aditya Pandya, Mikayla Deckard, Andrew J Munoz, Fred Bunz
{"title":"Robust p53 phenotypes and prospective downstream targets in telomerase-immortalized human cells.","authors":"Jessica J Miciak, Lucy Petrova, Rhythm Sajwan, Aditya Pandya, Mikayla Deckard, Andrew J Munoz, Fred Bunz","doi":"10.18632/oncotarget.28690","DOIUrl":"10.18632/oncotarget.28690","url":null,"abstract":"<p><p>Cancers that retain wild type <i>TP53</i> presumably harbor other clonal alterations that permitted their precursors to bypass p53-mediated growth suppression. Consequently, studies that employ <i>TP53</i>-wild type cancer cells and their isogenic derivatives may systematically fail to appreciate the full scope of p53 functionality. Several <i>TP53</i> phenotypes are known to be absent in the widely used isogenic HCT116 colorectal cancer (CRC) model, which originated from a tumor that had retained wild type <i>TP53</i>. In contrast, we show that restoration of p53 in the <i>TP53</i>-mutant CRC cell line DLD-1 impeded cell proliferation, increased levels of senescence and sensitized cells to ionizing radiation (IR). To study p53 in a non-cancer context, we disrupted <i>TP53</i> in hTERT-RPE1 cells. Derived from primary cells that were immortalized <i>in vitro</i>, hTERT-RPE1 expressed striking p53-dependent phenotypes and appeared to select for p53 loss during routine culture. hTERT-RPE1 expressed a p53-responsive transcriptome that was highly representative of diverse experimental systems. We discovered several novel downstream p53 targets of potential clinical relevance including <i>ALDH3A1</i>, which is involved in the detoxification of aldehydes and the metabolism of reactive oxygen species, and <i>nectin cell adhesion molecule 4</i> (<i>NECTIN4</i>) which encodes a secreted surface protein that is overexpressed in many tumors.</p>","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"79-100"},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143449674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Could Panitumumab with very low dose Capecitabine be an option as a maintenance regimen. 帕尼珠单抗与低剂量卡培他滨是否可以作为维持方案的一种选择。
Oncotarget Pub Date : 2025-02-12 DOI: 10.18632/oncotarget.28687
Doaa A Gamal, Aiat Morsy, Mervat Omar
{"title":"Could Panitumumab with very low dose Capecitabine be an option as a maintenance regimen.","authors":"Doaa A Gamal, Aiat Morsy, Mervat Omar","doi":"10.18632/oncotarget.28687","DOIUrl":"10.18632/oncotarget.28687","url":null,"abstract":"<p><strong>Background: </strong>Anti-epidermal growth factor receptor therapy showed an overall median survival improvement in <i>wild type Ras</i> metastatic colorectal cancer. Maintenance with anti <i>EGFR</i> in metastatic colorectal cancer wild type <i>Ras</i> was studied in many trials with promising results and many of these trials gave combined chemo with the target therapy and this combination had shown benefit in the form of synergistic effect and in delaying the resistance to the anti <i>EGFR</i>.</p><p><strong>Method: </strong>In our study patients received 6 cycles of 5-FU based chemotherapy with Panitumumab and patients who had partial response, complete response or stationary disease received metronomic Capecitabine with Panitumumab every 2 weeks for one year. The primary end point was progression free survival (PFS) and the secondary end points were safety, toxicity and overall survival (OS).</p><p><strong>Results: </strong>The median PFS for all patients was 18 ± 1.4 months and the median OS was 45 months. Patients with synchronous metastasis and those who received Oxaliplatin based regimen with Panitumumab were found to have longer PFS compared to those with metachronous metastasis or those who received other chemotherapy regimen with accepted toxicity profile to the maintenance therapy.</p><p><strong>Conclusion: </strong>Using Panitumumab with metronomic Capecitabine is considered an accepted maintenance regimen in wild type <i>Ras</i> metastatic colorectal cancer regardless of the primary site.</p>","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"67-78"},"PeriodicalIF":0.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11823472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143409754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types. SETDB1在骨肉瘤中的扩增:从其在健康组织和其他癌症类型中的作用来看
Oncotarget Pub Date : 2025-02-12 DOI: 10.18632/oncotarget.28688
Elodie Verdier, Nathalie Gaspar, Maria Eugenia Marques Da Costa, Antonin Marchais
{"title":"SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.","authors":"Elodie Verdier, Nathalie Gaspar, Maria Eugenia Marques Da Costa, Antonin Marchais","doi":"10.18632/oncotarget.28688","DOIUrl":"10.18632/oncotarget.28688","url":null,"abstract":"<p><p>Epigenetic modifications, which reversibly regulate gene expression without altering the DNA sequence, are increasingly described in the literature as essential elements in the processes leading to cancer development. SETDB1 regulates histone 3 (H3) K9 di- and trimethylation, promoting heterochromatin formation, and plays a key role in gene silencing. Epigenetic deregulation of <i>SETDB1</i> expression appears to be involved in different cancers types, particularly in aggressive, relapsing or treatment-resistant subtypes. Despite advances in research, the full range of mechanisms through which this protein acts remains unclear; however, it is evident that SETDB1 has a pivotal role, particularly in the mesenchymal stem cells differentiation, tumor evasion and treatment resistance. Its role in genetically complex sarcomas, such as osteosarcoma, has not been fully explored, although recent Omics analyses suggest its presence and amplification in osteosarcoma. Given its involvement in osteoblastogenesis and adipogenesis, we discuss the potential of SETDB1 as a key target for new therapeutic strategies in osteosarcoma.</p>","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"51-62"},"PeriodicalIF":0.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11823473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143409755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction: Catalytic inhibitors of DNA topoisomerase II suppress the androgen receptor signaling and prostate cancer progression. 更正:DNA拓扑异构酶II的催化抑制剂抑制雄激素受体信号传导和前列腺癌的进展。
Oncotarget Pub Date : 2025-02-12 DOI: 10.18632/oncotarget.28692
Haolong Li, Ning Xie, Martin E Gleave, Xuesen Dong
{"title":"Correction: Catalytic inhibitors of DNA topoisomerase II suppress the androgen receptor signaling and prostate cancer progression.","authors":"Haolong Li, Ning Xie, Martin E Gleave, Xuesen Dong","doi":"10.18632/oncotarget.28692","DOIUrl":"10.18632/oncotarget.28692","url":null,"abstract":"","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"63-64"},"PeriodicalIF":0.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11823470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143409751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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