OncoTargets and therapy最新文献

{"title":"Roles of SPOCK1 in the Formation Mechanisms and Treatment of Non-Small-Cell Lung Cancer and Brain Metastases from Lung Cancer.","authors":"Xuebing Zhang, Xia Zhang, Hang Yin, Qizheng Li, Buqun Fan, Bolun Jiang, Anqi Xie, Dandan Guo, Huanling Hao, Bin Zhang","doi":"10.2147/OTT.S483576","DOIUrl":"10.2147/OTT.S483576","url":null,"abstract":"<p><p>Lung cancer is a malignant tumor with high morbidity and mortality in China and worldwide. Once it metastasizes to the brain, its prognosis is very poor. Brain metastases are found in about 20% of newly diagnosed non-small-cell lung cancer (NSCLC) patients. About 30% of NSCLC patients develop brain metastases during treatment. NSCLC that is positive for EGFR, ALK, and ROS1 variations is especially likely to metastasize to the brain. SPOCK1 is a proteoglycan with systemic physiological functions. It regulates the self-renewal of brain metastasis-initiating cells, regulates invasion and metastasis from the lung to the brain, plays an important role in tumor progression and treatment resistance, and has higher expression in metastatic tumor tissues than other tissues. Current treatments for NSCLC brain metastases include surgery, whole-brain radiotherapy, stereotactic radiotherapy, targeted therapy, and chemotherapy. SPOCK1 is involved in many signaling pathways, by which it influences a variety of NSCLC treatment methods. In this paper, the progress of research on the treatment of NSCLC brain metastases is reviewed to guide decisions on treatment options in clinical practice.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"35-47"},"PeriodicalIF":2.7,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11745074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009048","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 Network Pharmacology, Machine Learning and Experimental Validation to Identify the Key Targets and Compounds of <i>TiaoShenGongJian</i> for the Treatment of Breast Cancer.","authors":"Huiyan Ying, Weikaixin Kong, Xiangwei Xu","doi":"10.2147/OTT.S486300","DOIUrl":"10.2147/OTT.S486300","url":null,"abstract":"<p><strong>Background: </strong>TiaoShenGongJian (TSGJ) decoction, a traditional Chinese medicine for breast cancer, has unknown active compounds, targets, and mechanisms. This study identifies TSGJ's key targets and compounds for breast cancer treatment through network pharmacology, machine learning, and experimental validation.</p><p><strong>Methods: </strong>Bioactive components and targets of TSGJ were identified from the TCMSP database, and breast cancer-related targets from GeneCards, PharmGkb, and RNA-seq datasets. Intersection of these targets revealed therapeutic targets of TSGJ. PPI analysis was performed via STRING, and machine learning methods (SVM, RF, GLM, XGBoost) identified key targets, validated by GSE70905, GSE70947, GSE22820, and TCGA-BRCA datasets. Pathway analyses and molecular docking were performed. TSGJ and core compounds' effectiveness was confirmed by MTT and RT-qPCR assays.</p><p><strong>Results: </strong>160 common targets of TSGJ were identified, with 30 hub targets from PPI analysis. Five predictive targets (HIF1A, CASP8, FOS, EGFR, PPARG) were screened via SVM. Their diagnostic, biomarker, immune, and clinical values were validated. Quercetin, luteolin, and baicalein were identified as core components. Molecular docking confirmed their strong affinities with predicted targets. These compounds modulated key targets and induced cytotoxicity in breast cancer cell lines in a similar way as TSGJ.</p><p><strong>Conclusion: </strong>This study reveals the main active components and targets of TSGJ against breast cancer, supporting its potential for breast cancer prevention and treatment.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"49-71"},"PeriodicalIF":2.7,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11745062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Rare Case of Post-Transplant Lymphoproliferative Disorder Presenting as Hodgkin Lymphoma After Autologous Hematopoietic Stem Cell Transplantation: A Case Report and Literature Review.","authors":"Yuzhan Chen, Ying Chen, Yimin He, Qitian Mu, Guifang Ouyang","doi":"10.2147/OTT.S490591","DOIUrl":"10.2147/OTT.S490591","url":null,"abstract":"<p><p>Post-transplant lymphoproliferative disorder (PTLD) is a rare complication following hematopoietic stem cell transplantation (HSCT), with its occurrence post-autologous hematopoietic stem cell transplantation (auto-HSCT) being even rarer. Research on PTLD following auto-HSCT is exceedingly scarce. Here, we present a noteworthy instance wherein a patient with diffuse large B-cell lymphoma (DLBCL) developed PTLD, manifesting as classical Hodgkin lymphoma (cHL) two years after auto-HSCT. Additionally, we conducted an extensive review of existing literature, exploring the current research on PTLD following auto-HSCT and illuminating this scarcely examined area.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"27-33"},"PeriodicalIF":2.7,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009140","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":"High Intelectin-1 Expression Associated with Aggressive Tumor Behavior and Worse Survival in Rectal Cancer.","authors":"Chia-Lin Chou, Cheng-Wei Lin, Wan-Shan Li, Tzu-Ju Chen, Sung-Wei Lee, Yu-Feng Tian, Yu-Hsuan Kuo, Hsin-Hwa Tsai, Li-Ching Wu, Cheng-Fa Yeh, Yow-Ling Shiue, Hong-Yue Lai, Ching-Chieh Yang","doi":"10.2147/OTT.S488608","DOIUrl":"https://doi.org/10.2147/OTT.S488608","url":null,"abstract":"<p><strong>Background: </strong>Multimodal treatment involving preoperative chemoradiotherapy (CRT) followed by surgery is the current standard of care for rectal cancer. Despite advancements, the risk of recurrence, metastasis, and decreased survival remains high. This study aims to evaluate potential biomarkers to stratify prognosis in patients with rectal cancer undergoing preoperative CRT and surgery.</p><p><strong>Methods: </strong>Through data mining of receptor-binding pathways in a published transcriptome for rectal cancer cases, ITLN1 was identified as the most relevant gene associated with poor response to chemoradiation (GO:0005102). Rectal cancer specimens (n = 343) collected between 1998 and 2017 were analyzed for ITLN1 expression using immunohistochemistry. The association between ITLN1 protein expression and clinicopathological features was assessed using Pearson's chi-square test. Survival outcomes based on ITLN1 expression were evaluated using the Kaplan-Meier method and compared with Log rank tests.</p><p><strong>Results: </strong>ITLN1 immunoreactivity was significantly elevated in rectal tumor tissues. High ITLN1 expression was strongly associated with adverse clinicopathological features, including advanced post-treatment tumor status (T3-4; p = 0.001), post-treatment nodal status (N1-2; p < 0.001), vascular invasion (p = 0.017), perineural invasion (p = 0.001), and a lower degree of tumor regression (p = 0.009). Uni- and multivariable analyses revealed that high ITLN1 expression correlated with poorer disease-specific survival, local recurrence-free survival, and distant metastasis-free survival compared to low ITLN1 expression.</p><p><strong>Conclusion: </strong>Elevated ITLN1 expression is significantly associated with aggressive tumor behavior and unfavorable survival outcomes in rectal cancer. These findings highlight ITLN1 as a potential prognostic biomarker and provide a foundation for future research into its role in rectal cancer progression and treatment response.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"15-26"},"PeriodicalIF":2.7,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11740546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009142","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":"Recent Advances in Understanding the Clinical Responses of Brentuximab Vedotin in Lymphoma and the Correlation with CD30 Expression.","authors":"Wen Chen, Zhihong Zhang","doi":"10.2147/OTT.S487088","DOIUrl":"10.2147/OTT.S487088","url":null,"abstract":"<p><p>Brentuximab vedotin (BV) is an antibody-drug conjugate that combines the CD30 monoclonal antibody with the microtubule-disrupting agent, monomethyl auristatin E, which induces apoptosis in the tumor cell upon its release from the conjugate. The safety and efficacy of BV have been assessed in several studies in patients with T- and B-cell lymphomas. This article reviews the currently available data on the distribution of CD30 expression in T- and B-cell lymphomas, as well as the various levels of CD30 positivity cutoff used in the literature. It also analyzes the relationship between CD30 expression levels and the clinical response to BV in clinical trials for both T- and B-cell lymphomas and investigates BV efficacy in patients with low or undetectable levels of CD30 and examines potential mechanisms by which BV exerts its effect on these patients. This review contributes to the growing evidence suggesting that CD30 expression levels do not predict the clinical benefit of BV as the drug demonstrated substantial efficacy in patients across a wide range of CD30 expression levels while suggesting that the antitumor activity was not associated with CD30 expression levels. Furthermore, the potential of BV as a targeted approach along with its mechanism of action is also summarized to explain its key role in the future treatments of lymphomas, especially for CD30-expressing lymphomas.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"1-14"},"PeriodicalIF":2.7,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11720807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971748","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":"Progress of Immune Checkpoint Inhibitors Therapy for pMMR/MSS Metastatic Colorectal Cancer.","authors":"Fanjie Qu, Shuang Wu, WeiWei Yu","doi":"10.2147/OTT.S500281","DOIUrl":"10.2147/OTT.S500281","url":null,"abstract":"<p><p>Immunotherapy is one of the research hotspots in colorectal cancer field in recent years. The colorectal cancer patients with mismatch repair-deficient (dMMR) or high microsatellite instability (MSI-H) are the primary beneficiaries of immunotherapy. However, the vast majority of colorectal cancers are mismatch repair proficient (pMMR) or microsatellite stability (MSS), and their immune microenvironment is characterized by \"cold tumors\" that are generally insensitive to single immunotherapy based on immune checkpoint inhibitors (ICIs). Studies have shown that some pMMR/MSS colorectal cancer patients regulate the immune microenvironment by combining other treatments, such as multi-target tyrosine kinase inhibitors, anti-vascular endothelial growth factor (VEGF) monoclonal antibodies, chemotherapy, radiotherapy, anti-epithelial growth factor receptor (EGFR) monoclonal antibodies, and mitogen-activated protein kinase (MAPK) signaling pathway inhibitors and oncolytic viruses, etc. to transform \"cold tumor\" into \"hot tumor\", thereby improving the response to immunotherapy. In addition, screening for potential prognostic biomarkers can also enrich the population benefiting from immunotherapy for microsatellite stable colorectal cancer. Therefore, in pMMR or MSS metastatic colorectal cancer (mCRC), the optimization of immunotherapy regimens and the search for effective efficacy prediction biomarkers are currently important research directions. In this paper, we review the progress of efficacy of immunotherapy (mainly ICIs) in pMMR /MSS mCRC, challenges and potential markers, in order to provide research ideas for the development of immunotherapy for mCRC.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1223-1253"},"PeriodicalIF":2.7,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903347","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 a Prognostic Risk Model for Esophageal Cancer Based on M0 Macrophage-Related Genes.","authors":"Xiaoping Zuo, Fuqiang Wang, Guofeng Liu, Shenglong Xie, Senyi Deng, Yun Wang","doi":"10.2147/OTT.S483536","DOIUrl":"10.2147/OTT.S483536","url":null,"abstract":"<p><strong>Background: </strong>This study investigates the prognostic value of M0 macrophage-related genes (M0MRGs) in esophageal cancer (ESCA) and identifies novel targets for immunotherapy.</p><p><strong>Methods: </strong>Differentially expressed genes (DEGs) were screened with ESCA-related expression profile data (GSE5364 and GSE17351) from the GEO database, followed by GO and KEGG pathway enrichment analyses. Then, immune cell infiltration was examined with the CIBERSORT algorithm and multiplex fluorescence-based immunohistochemistry (MP-IHC). ESCA-related gene expression data and relevant clinical information were retrieved from TCGA. M0MRGs were identified with TCGA-ESCA based on Spearman's correlation coefficient. Additionally, LASSO and Cox regression analyses were conducted to further construct an M0MRG-related prognostic model. ATP6V0D2 and MMP12 expression in ESCA was analyzed with tissue microarray. Finally, the half maximal inhibitory concentrations (IC50) of commonly used chemotherapeutics in TCGA-ESCA were calculated with the \"oncoPredict\" R package.</p><p><strong>Conclusion: </strong>In summary, ATP6V0D2 and MMP12 were crucial components in a prognostic risk model for ESCA and were associated with poor prognoses, implicating the involvement of elevated M0 macrophages in disease progression and providing potential therapeutic targets and strategies for ESCA.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1209-1222"},"PeriodicalIF":2.7,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903345","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":"CRISPR-Cas13a Targeting the FGFR3-TACC3 Fusion Gene Inhibits Proliferation of Bladder Cancer Cells in vitro and in vivo.","authors":"Yadong Wang, Jinjin Zhu, Shangwen Liu, Zhengbo Sun, Guibiao Wen, Dakun Huang, Mianxiong Chen, Yuchen Liu, Feng Lin","doi":"10.2147/OTT.S492659","DOIUrl":"10.2147/OTT.S492659","url":null,"abstract":"<p><strong>Introduction: </strong>The FGFR3-TACC3 fusion gene exists in a variety of malignant tumors, including bladder cancer. In our ongoing research on the CRISPR-Cas13a gene-editing system, we reported the use of CRISPR-Cas13a gene-editing system to knockout FGFR3-TACC3 and inhibit the proliferation of bladder tumor cells.</p><p><strong>Purpose: </strong> This study aimed to use the CRISPR-Cas13a gene-editing system to target the FGFR3-TACC3 fusion gene in bladder cancer cells, which has the potential to be a new and effective treatment for bladder cancer.</p><p><strong>Materials and methods: </strong>The efficacy of the CRISPR-Cas13a gene-editing system was analysed by qRT-PCR. The inhibitory effects of Cas13a-mediated knockdown of the FGFR3-TACC3 fusion gene on the proliferation of RT4 and RT112 cell lines were assessed utilizing CCK-8, EdU, and organoid formation assays. Subsequently, the comparative tumorigenic capability of RT4 cells with FGFR3-TACC3 knockdown achieved by Cas13a was examined in a nude mouse model.</p><p><strong>Results: </strong>At the cellular level, the comparative analysis of FGFR3-TACC3 knockdown efficacy between CRISPR-Cas13a and shRNA revealed a more pronounced reduction with the former. This knockdown effectively curtailed cellular proliferation, with CRISPR-Cas13a-mediated knockdown exhibiting a superior inhibitory effect over shRNA-mediated knockdown. In organoid cultures derived from RT4 cells, a similar trend was observed, with Cas13a-mediated knockdown of FGFR3-TACC3 leading to a more substantial suppression of proliferation compared to shRNA-mediated knockdown. In vivo tumor models corroborated these findings, demonstrating a significantly diminished tumor volume in the Cas13a-treated cohort relative to both the control and shRNA-treated groups.</p><p><strong>Conclusion: </strong>The CRISPR-Cas13a gene-editing system has been demonstrated to significantly suppress tumor proliferation both in vitro and in vivo, thereby presenting itself as a promising candidate for a novel and efficacious therapeutic intervention in bladder cancer treatment.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1197-1207"},"PeriodicalIF":2.7,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882324","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":"Erratum: Long Non-Coding RNA TRG-AS1 Promoted Proliferation and Invasion of Lung Cancer Cells Through the miR-224-5p/SMAD4 Axis [Retraction] [Corrigendum].","authors":"","doi":"10.2147/OTT.S511815","DOIUrl":"10.2147/OTT.S511815","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.2147/OTT.S474055.].</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1195-1196"},"PeriodicalIF":2.7,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11662905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876899","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":"Silencing of Long Noncoding RNA LINC00346 Inhibits the Tumorigenesis of Colorectal Cancer Through Targeting MicroRNA-148b [Retraction].","authors":"","doi":"10.2147/OTT.S511336","DOIUrl":"https://doi.org/10.2147/OTT.S511336","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.2147/OTT.S242715.].</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1187-1188"},"PeriodicalIF":2.7,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11648281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838737","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}