OncoTargets and therapy最新文献

{"title":"Influence of Human Papillomavirus E6 Gene Mutation on Brain-Derived Neurotrophic Factor Regulation and Cell Proliferation in Cervical Neoplasia: Insights Into Molecular Mechanisms.","authors":"Ling Wei, Qian Yu, Su-Ning Chen","doi":"10.2147/OTT.S488976","DOIUrl":"10.2147/OTT.S488976","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects and mechanisms of human papillomavirus E6 (HPV16 E6) gene mutation on cervical cancer and cervical intraepithelial neoplasia grade I (CIN I) cell proliferation by regulating brain-derived neurotrophic factor (BDNF).</p><p><strong>Methods: </strong>Real-time PCR was employed to measure mRNA levels of HPV16 E6 T350G, BDNF, and p53 in cervical cancer and CIN I tissues. Lentiviral vectors (pLV5-HPV16 E6 T350G and pLV5-vector) were constructed and transfected into human cervical epithelial cells. Real-time PCR validated successful infection and assessed mRNA changes induced by HPV16 E6 T350G. Western Blot was used to detect BDNF protein levels and PI3K/AKT phosphorylation. Cell proliferation was evaluated with the MTT assay, a standard method for assessing cell viability in vitro.</p><p><strong>Results: </strong>Compared with CIN I cervical tissue, HPV16 E6 T350G and BDNF mRNA expression levels were positive in cervical cancer tissue, while p53 mRNA expression was negative; overexpression of HPV16 E6 T350G in human cervical epithelial cells upregulated BDNF mRNA and protein expression and activated its downstream signaling pathway PI3K/AKT, while reducing p53 protein expression; overexpression of HPV16 E6 T350G enhanced the proliferation ability of human cervical epithelial cells.</p><p><strong>Conclusion: </strong>Overexpression of HPV16 E6 T350G can promote the proliferation ability of cervical cancer cells, possibly by upregulating BDNF expression to promote activation of the PI3K/AKT signaling pathway and decrease p53 expression.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"1083-1091"},"PeriodicalIF":2.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12474662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186224","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":"Ebp1 p48 Promotes Oncogenic Properties in Non-Small Cell Lung Cancer Through PI3K/Akt Signaling Pathways.","authors":"Lina Ma, Shuyuan Wang, Jia Zhang, Mengyuan Xin, Dongyuan Xu, Lan Liu, Xiangdan Li","doi":"10.2147/OTT.S537306","DOIUrl":"10.2147/OTT.S537306","url":null,"abstract":"<p><strong>Purpose: </strong>Lung cancer, particularly non-small cell lung cancer (NSCLC), is highly deadly globally. The potential carcinogenic role of p48, a long isoform of ErbB3-binding protein 1 (Ebp1), is well established in other cancers, but its impact on NSCLC remains unconfirmed.</p><p><strong>Patients and methods: </strong>Several databases were utilized to compare Ebp1 expression in normal lung and NSCLC. Immunohistochemical staining was employed to identify Ebp1 expression in both types of tissue. The TCGA database assessed Ebp1 expression in NSCLC and its impact on overall survival. Ebp1 expression was knocked down in A549 and PC9 cells, and the impact of Ebp1 on the cell growth was tested by CCK-8, plate clone colony, soft agar colony generation assay, and cell cycle assays. Scratch, transwell, and in vivo were also used to confirm the effects of Ebp1 on Lung cancer cells migration, invasion. Western blot detection of EMT and signal pathway-related proteins.</p><p><strong>Results: </strong>This study revealed that NSCLC had significantly higher levels of Ebp1 p48 expression. We discovered a correlation between Ebp1 p48 expression and pathological grade, lymph node metastasis, clinical stage, and overall survival (OS) using NSCLC tissue microarrays. In vitro and in vivo tumor cell growth, migration, invasion, the epithelial-mesenchymal transition (EMT) process, and cell proliferation are all markedly suppressed when Ebp1 p48 is knocked down in NSCLC cells. Moreover, PI3K and Akt phosphorylation levels were decreased by Ebp1 p48 knockdown.</p><p><strong>Conclusion: </strong>According to these findings, Ebp1 p48 stimulated the PI3K/Akt signaling pathway in NSCLC, which in turn facilitated invasion, migration, and proliferation. As a result, in NSCLC, Ebp1 p48 may be a prospective therapeutic target as well as a predictive biomarker.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"1093-1105"},"PeriodicalIF":2.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12474717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186300","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":"Vitamin C Selectively Inhibits Kidney Renal Clear Cell Carcinoma Cell Growth by Suppressing the HIF-1 Pathway.","authors":"Che Wang, Yaoyang Zhou, Yu Liang, Jue Pan, Jinyu Qiao, Lingbo Chen, Silin Liu, Jie Chen, Jin Wang, Xiao Sun, Jinlu Ma, Mengjiao Cai","doi":"10.2147/OTT.S512698","DOIUrl":"10.2147/OTT.S512698","url":null,"abstract":"<p><strong>Aim: </strong>To observe the effect of vitamin C on Kidney renal clear cell carcinoma (KIRC) and investigate its mechanism.</p><p><strong>Methods and results: </strong>Firstly, 29 vitamin C direct target proteins (DPTs) were identified by Drug Bank 5.0, and the protein-protein interaction (PPI) network and signaling pathways of vitamin C DPTs were analyzed. The results showed that vitamin C was not only related to KIRC, but also to the HIF-1 pathway. Meanwhile, the top 300 highly expressed genes of KIRC were obtained by GEPIA. Next, We compared the genes of four vitamin C targets in the PPI network with highly expressed genes in KIRC. Interestingly, these common genes are also involved in HIF-1 pathway. Additionally, we utilized RNA-Seq technology to explore the differentially expressed genes in KIRC with vitamin C compared to those not intervened. We observed that these differentially expressed genes exhibited a close association with hypoxia. Finally, we observed the inhibitory effect of Vitamin C on KIRC by Cell Counting Kit-8 (CCK8) assay, real-time quantitative PCR, Western blotting, flow cytometry, and colony formation assay, and confirmed that Vitamin C inhibits the growth of KIRC cells through the HIF-1 pathway.</p><p><strong>Conclusion: </strong>Through bioinformatics analyses, we identified the molecular mechanism of vitamin C's role in KIRC and verified it through a series of experiments. Combined bioinformatics analysis will play an important role in future drug-disease interaction studies.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"1069-1081"},"PeriodicalIF":2.8,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12459377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150297","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":"Serum Response Factor Expression, Microvascular Density, and Postoperative Recurrence in Glioblastoma.","authors":"Bo Tan, Shuangyin He, Tao Chen, Peng Song, Yaohui Huang, Xiaohong Yin","doi":"10.2147/OTT.S546017","DOIUrl":"10.2147/OTT.S546017","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the association between serum response factor (SRF) expression, tumour microvascular density (MVD), and postoperative recurrence in glioblastoma.</p><p><strong>Methods: </strong>This retrospective study analysed 92 patients with histologically confirmed glioblastoma treated between July 2021 and July 2023. Tumour and adjacent normal brain tissues were collected during surgery for immunohistochemical detection of SRF and CD105. MVD was determined by counting CD105-positive microvessels in the most vascularised tumour regions. Spearman correlation assessed the association between SRF and MVD. All patients underwent maximal surgical resection and were followed for 1 year. Recurrence was defined by MRI. Multivariate logistic regression identified independent predictors of recurrence.</p><p><strong>Results: </strong>SRF-positive tumours were significantly more frequent than in adjacent normal brain tissue (56.5% vs 2.2%, P<0.001) and had higher MVD (86.79 ± 14.12 vs 70.58 ± 8.77 vessels/field, P<0.05). SRF expression correlated positively with MVD (r = 0.749, P<0.05). At 1 year, 24 patients (26.1%) recurred. Compared with non-recurrent cases, the recurrence group had higher rates of SRF positivity, tumour size ≥5 cm, poor differentiation, high grade, and incomplete resection (all P<0.05). Multivariate analysis identified SRF positivity, tumour size ≥5 cm, poor differentiation, high grade, and incomplete resection as independent recurrence predictors.</p><p><strong>Conclusion: </strong>SRF overexpression in glioblastoma is associated with increased angiogenesis and higher recurrence risk. SRF may promote tumour proliferation, differentiation, and migration, and serve as a prognostic biomarker and potential therapeutic target.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"1043-1052"},"PeriodicalIF":2.8,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145138234","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":"Could Silent Inflammation Originating in Jawbone Cavitations Play a Role in Activating the CCL5/CCR5 Axis in Female Breast Cancer? A Diagnostic and Therapeutic Gap in Osteoimmunological Interactions.","authors":"Joana Vasconcelos E Cruz, Sebastjan Perko, Cornelia Doebis, Florian Notter, Fabian Schick, Johann Lechner","doi":"10.2147/OTT.S526033","DOIUrl":"10.2147/OTT.S526033","url":null,"abstract":"<p><strong>Introduction: </strong>Breast cancer (BC) is one of the leading causes of cancer mortality worldwide. The chemokine CCL5 and its receptor CCR5 have been demonstrated to be associated with tumour progression, immune evasion, and metastasis.</p><p><strong>Objective: </strong>Recent evidence indicates that chronic inflammatory conditions in the jawbone, specifically fatty degenerative osteonecrosis of the jaw (FDOJ), may serve as a continuous source of CCL5 overexpression, potentially influencing BC development.</p><p><strong>Methods: </strong>This multicentre study, conducted in Germany, Portugal and Slovenia, investigated the correlation between FDOJ-related CCL5 expression and BC. Patients undergoing surgical removal of FDOJ areas were examined using advanced imaging (trans alveolar ultrasonography) and multiplex cytokine analysis to detect bone marrow defects and measure CCL5 levels.</p><p><strong>Results: </strong>The results demonstrated a marked increase in CCL5 expression in FDOJ samples in comparison to healthy jawbone tissue.</p><p><strong>Discussion: </strong>Statistical analysis revealed a strong correlation between FDOJ and elevated CCL5, thereby supporting the hypothesis that jawbone inflammation may activate the CCL5/CCR5 axis in BC patients. This finding suggests that FDOJ may represent an underrecognized inflammatory comorbidity that contributes to BC progression.</p><p><strong>Conclusion: </strong>The study under discussion highlights a hitherto unidentified osteoimmune mechanism that links inflammation of the jawbone to cancer pathways. It also emphasizes the potential benefit of targeted surgical interventions such as \"Jawbone Detox^®\" in reducing chronic CCL5 levels. Such approaches have the potential to offer novel preventive and therapeutic options for patients diagnosed with BC. Further clinical studies are required to confirm the effects of FDOJ treatment on immune function and BC outcomes.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"1053-1068"},"PeriodicalIF":2.8,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12457831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150276","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":"Glycolysis-Driven Immune Evasion in Microsatellite Instability-High Colorectal Cancer: An Integrated Single-Cell and Spatial Transcriptomics Study.","authors":"Chenchen Li, Peicong Cai, Hengda Zeng, Jianxia Li, Huabin Hu, Jianwei Zhang, Zehua Wu, Ge Qin, Yanhong Deng","doi":"10.2147/OTT.S538018","DOIUrl":"10.2147/OTT.S538018","url":null,"abstract":"<p><strong>Purpose: </strong>Microsatellite instability-high colorectal cancer is characterized by hypermutated genomes and high neoantigen loads, yet a significant proportion of patients exhibit resistance to immune checkpoint blockade. This study aims to investigate tumor cell functional heterogeneity and its role in immune evasion.</p><p><strong>Patients and methods: </strong>We integrated single-cell RNA sequencing, spatial transcriptomics, and bulk RNA sequencing from microsatellite instability-high colorectal cancer patients. After quality control, normalization, and clustering, malignant epithelial subpopulations were identified through copy number variation analysis and non-negative matrix factorization. Functional characterization employed gene set enrichment analysis. Spatial transcriptomics clarified immune cell and tumor subpopulation localization, and survival analyses assessed prognostic implications.</p><p><strong>Results: </strong>We identified a glycolysis-enriched tumor subpopulation (MP2) that co-localized with immunosuppressive niches marked by Treg accumulation, effector T-cell depletion, and FOLR2+ tumor-associated macrophages. MP2-high tumors were associated with immune checkpoint blockade resistance and poor prognosis. Mechanistically, MP2 cells secreted lactate, promoting Treg differentiation and macrophage polarization toward an immunosuppressive phenotype. Spatial transcriptomics revealed the precise organization of these lactate-rich, immune-excluded niches within tumors.</p><p><strong>Conclusion: </strong>These findings establish tumor cell-intrinsic glycolysis as a key driver of immune evasion in microsatellite instability-high colorectal cancer and propose metabolic targeting as a strategy to overcome immune checkpoint blockade resistance.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"1027-1042"},"PeriodicalIF":2.8,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12452990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131486","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":"Can Epithelial-Myoepithelial Carcinoma of the Breast Benefit from TROP2 Antibody-Drug Conjugate?","authors":"Qing Zhao, Xiao Luo, Hua Xing, Chengwei Jiang, Jingchao Ma, Lu Tang","doi":"10.2147/OTT.S540295","DOIUrl":"10.2147/OTT.S540295","url":null,"abstract":"<p><p>Epithelial-myoepithelial carcinoma (EMC) of the breast is a rare biphasic tumor composed of intermixed malignant epithelial and myoepithelial components. Breast epithelial myoepithelial carcinoma lacks therapeutic strategies due to its rarity, and currently local treatment is still the main treatment. Herein we report an epithelial-myoepithelial carcinoma of the breast in a 33-year-old woman undergoing breast conserving surgery, sentinel lymph node biopsy, adjuvant chemotherapy and radiotherapy, with rapid liver and lung metastasis. After radiofrequency ablation therapy for metastatic lesions, vinorelbine plus cisplatin and TROP2 antibody-drug conjugate (ADC) treatment were given successively. After a brief improvement, drug resistance developed and the disease progressed. The patient died with the PFS 5.6 months.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"1013-1025"},"PeriodicalIF":2.8,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12439690/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081275","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 Immunomodulatory Activity of Thymosin Alpha 1 on Tumor Cell Lines and Distinct Immune Cell Subsets.","authors":"Laura Solmonese, Maria Fortunata Lofiego, Carolina Fazio, Francesco Marzani, Francesca Piazzini, Emma Bello, Fabrizio Celesti, Gianluca Giacobini, Xiaohui Wang, Michele Maio, Sandra Coral, Anna Maria Di Giacomo, Alessia Covre","doi":"10.2147/OTT.S527785","DOIUrl":"10.2147/OTT.S527785","url":null,"abstract":"<p><strong>Background: </strong>The immune-balancing role of thymosin alpha 1 (Tα1) is well-recognized in contexts of immune dysregulation. Within the anti-tumor context, Tα1 demonstrated to act as an immune-enhancer, with potential roles in immunotherapy-based treatments. However, Tα1 immunomodulatory potential on tumor cells is poorly understood. Additionally, Tα1 pleiotropic effects on immune cells require in-depth investigations to unravel its specific impact on different immune cell populations. Thus, we first aimed to investigate whether Tα1 treatments influenced the transcriptional immune profile of various cancer cell lines. Alongside, CD4⁺ T, CD8⁺ T, B, and natural killer cells from healthy donors (HDs) were treated individually with Tα1, to assess its direct effects on each immune cell population.</p><p><strong>Methods: </strong>Cutaneous melanoma, glioblastoma, and pleural mesothelioma cell lines and HD immune cell subsets were treated with Tα1 for 48 hours. Total RNA was subsequently isolated, and gene expression profiles were analyzed by the nCounter^® SPRINT Profiler. Genes with a log2ratio ≥0.58 and ≤-0.58 in Tα1-treated vs untreated cells were defined as differentially expressed (DEGs) and subsequently evaluated for the enrichment of Gene Ontology terms to identify biological processes potentially affected by Tα1 in tumor and immune cells.</p><p><strong>Results: </strong>Tα1 minimally changed cancer cell DEGs and immune-related biological processes, suggesting a comprehensive lack of transcriptional immunomodulatory potential on the tumor counterpart. Conversely, Tα1 exhibited to directly affect the proliferation and/or transcription processes of each studied immune cell subset, with the greatest transcriptional impact observed for activated CD8⁺ T cells, crucial players in anti-tumor immunity.</p><p><strong>Conclusion: </strong>Our findings question the tumor immunomodulatory properties of Tα1, simultaneously underscoring the importance of further investigating Tα1 influence on specific immune cell subsets in the periphery or within the tumor microenvironment of cancer patients. This would contribute to understand Tα1 potential in immunotherapy-based combination strategies, within the anti-tumor setting.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"995-1012"},"PeriodicalIF":2.8,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12433645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069958","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 Dual Role of RBBP7 in Esophageal Squamous Cell Carcinoma: Cell Context-Dependent Impacts on Proliferation and Radiosensitivity.","authors":"Yafen Li, Shuai Lu, Hui Yao, Genbao Zhu, Hao Liu, Zhiyu Ma, Heng Tang","doi":"10.2147/OTT.S535750","DOIUrl":"10.2147/OTT.S535750","url":null,"abstract":"<p><strong>Background: </strong>Radiotherapy resistance contributes to poor prognosis in esophageal squamous cell carcinoma (ESCC). Retinoblastoma-binding protein 7 (RBBP7) is a nuclear protein, and it can promote or inhibit tumor progression in cancer, but its function in ESCC cells and impact on radiosensitivity remains unclear.</p><p><strong>Methods: </strong>RBBP7 expression in cancer was analyzed using an online website. The expression levels of RBBP7 in ESCC cells (TE-1 and KYSE-150) and tissues were tested. Cells were subjected to RBBP7 gene silencing and irradiation (IR). Assays included CCK-8, clonogenic survival, flow cytometry (apoptosis/cell cycle), ROS detection, and Western blotting for DNA damage (γ-H2AX) and STAT3 signaling. Additionally, pathological tissue specimens and clinical data from ESCC patients were used to explore the expression of RBBP7.and its relationship with the clinical parameters of patients.</p><p><strong>Results: </strong>RBBP7 was overexpressed in malignant tumors. In ESCC cells, the mRNA and protein of RBBP7 were also highly expressed. After silencing RBBP7 combined with IR treatment, contradictory effects were observed between cell lines: In well-differentiated TE-1 cells, RBBP7 knockdown suppressed proliferation, enhanced radiosensitivity (SER=1.370), increased ROS/DNA damage (γ-H2AX), promoted apoptosis, and reduced STAT3 activation (possibly through STAT3 signaling). In poorly-differentiated KYSE-150 cells, knockdown promoted proliferation, decreased radiosensitivity (SER=0.775), reduced apoptosis, and increased p-STAT3. In addition, knockdown caused S-phase arrest (TE-1) versus G0/G1 arrest (KYSE-150), with divergent CDK4/Cyclin D1 regulation. Clinical analysis confirmed RBBP7 positivity correlated with tumor differentiation, TNM stage, and radiotherapy method.</p><p><strong>Conclusion: </strong>RBBP7 is highly expressed in ESCC, and it exerts cell context-dependent dual roles in ESCC, leading to differences in cellular radiosensitivity, possibly mediated through STAT3 signaling. This dichotomy highlights its potential as a differentiation status-specific therapeutic target.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"979-994"},"PeriodicalIF":2.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12417692/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040924","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":"Mi-Lnc70 Regulates the Progression of Murine Pancreatic β-Cell Line and Affects the Synthesis of Insulin and Glucagon.","authors":"Wen Yuan, Dongxue Sun, Jing Wang, Yongli Yue, Xueling Li","doi":"10.2147/OTT.S523599","DOIUrl":"10.2147/OTT.S523599","url":null,"abstract":"<p><strong>Background: </strong>Insulinoma, the most common type of pancreatic endocrine tumor, frequently induces hypoglycemia due to persistent hyperinsulinemia. Although Mi-Lnc70 expression progressively increases during pancreatic maturation in mice, the biological role of Mi-Lnc70 in pancreatic β cells remains elusive.</p><p><strong>Aim: </strong>This study was designed to investigate the role of LncRNA-Mi-Lnc70 in the mouse pancreatic β-cell line MIN6.</p><p><strong>Methods: </strong>We performed quantitative real-time PCR, cell counting kit-8 (CCK-8) assay, flow cytometry, transwell assay, wound healing assay, immunofluorescence staining, and Western blotting.</p><p><strong>Results: </strong>The expression of Mi-Lnc70 was markedly elevated in mouse pancreatic β-cells (MIN6) compared to normal cells. Knockdown of Mi-Lnc70 markedly suppressed the proliferation, migration, and invasion capabilities of MIN6 cells but induced cell apoptosis and triggered G2/M phase cell cycle arrest. Moreover, Mi-Lnc70 knockdown influenced the expression profiles of pancreas-related lncRNAs and miRNAs and decreased the expression of islet-related genes and reduced the protein synthesis of INSULIN, GLUCAGON, and PDX1.</p><p><strong>Conclusion: </strong>Mi-Lnc70 plays an important role in the proliferation, migration, and endocrine-related gene expression in pancreatic MIN6 cells, particularly in the synthesis of PDX1, INSULIN, and GLUCAGON.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"967-978"},"PeriodicalIF":2.8,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12415100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145030207","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}