Cancer Biology & Therapy最新文献

{"title":"Neoplastic CD3⁺ B cells remodel the DLBCL tumor microenvironment via single-cell and spatial transcriptomics.","authors":"Mingxiao Lang, Youqin Feng, Li Zhou, Bin Li, Wei Li, Jing Zhao, Kexin Chen, Lanfang Li, Lihua Qiu, Zhengzi Qian, Shiyong Zhou, Huilai Zhang, Zhaobin Chu","doi":"10.1080/15384047.2026.2684140","DOIUrl":"10.1080/15384047.2026.2684140","url":null,"abstract":"<p><strong>Introduction: </strong>This study constructs a high-resolution multi-omics map of Diffuse Large B-Cell Lymphoma (DLBCL) by integrating single-cell, single-nucleus, and spatial transcriptomics.</p><p><strong>Methods: </strong>We identified a previously unrecognized, recurrent subset of malignant B cells that unexpectedly express CD3, a protein typically found only on T cells. This unusual CD3⁺ B cell population appears to be driven by a specific genetic circuit involving five key regulatory genes: BCLAF1, CHURC1, FLI1, NFATC2, and ELF2.</p><p><strong>Result: </strong>Spatial and functional analyses revealed that these cells are associated with macrophage enrichment and M2 polarization, potentially involving TGF-<i>β</i> signaling and contributing to an immunosuppressive tumor microenvironment. Clinically, the abundance of CD3⁺ B cells was associated with advanced disease stage, poor treatment response, and reduced survival.</p><p><strong>Conclusion: </strong>Our findings support the presence of a CD3⁺ B cell subset with T cell-like features that is associated with tumor microenvironment remodeling and adverse clinical outcomes, highlighting molecular determinants like FLI1 and the TGF-<i>β</i> axis as potential therapeutic targets.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2684140"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13245064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148175547","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":"Targeting the PI3K/AKT pathway in prostate cancer: the role of PTEN deficiency and biomarker-guided therapy.","authors":"Allison Staton, Melissa Abel, William D Figg","doi":"10.1080/15384047.2026.2694128","DOIUrl":"10.1080/15384047.2026.2694128","url":null,"abstract":"<p><p>Loss of the <i>PTEN</i> tumor suppressor gene is a common molecular feature in advanced prostate cancer and is associated with activation of the PI3K/AKT signaling pathway, which controls cell growth and survival. Despite major advances in the treatment of metastatic castration-sensitive prostate cancer (mCSPC), patients with PTEN-deficient tumors represent an aggressive subgroup with poorer clinical outcomes and limited targeted therapeutic options. Capivasertib is a selective oral AKT inhibitor designed to suppress downstream signaling from PI3K pathway activation. We highlight the recent results from the Phase III CAPItello-281 trial (NCT04493853) demonstrating that the addition of capivasertib to abiraterone acetate and androgen deprivation therapy (ADT) significantly improved radiographic progression-free survival in patients with <i>PTEN</i>-deficient mCSPC, leading to the FDA-approval of this regimen. Notable adverse events in the cabavisertib arm included hyperglycemia, diarrhea, and rash. CAPItello-281 addresses a significant unmet need for <i>PTEN</i>-deficient mCSPC, suggesting AKT inhibition as a potential new targeted treatment strategy for a sub-population with poor prognosis.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2694128"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13313236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148326955","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":"Opsonization and timing as key determinants of MBTA immunotherapy efficacy in pancreatic adenocarcinoma and recurrence treatment.","authors":"Andrea Frejlachova, Radka Lencova, Ondrej Uher, Katerina Hadrava Vanova, Klara Martinkova, Monika Cizkova, David Vetvicka, Helena Langhansova, Jan Kopecky, Karel Pacak, Jan Zenka","doi":"10.1080/15384047.2026.2683273","DOIUrl":"10.1080/15384047.2026.2683273","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic adenocarcinoma is a highly aggressive cancer with very limited treatment options. This study aimed to optimize the efficacy of a previously developed tumor immunotherapy for the treatment of this disease and its recurrences.</p><p><strong>Methods: </strong>Mouse models of pancreatic and colon adenocarcinoma were established using Panc02 and MC38 cells, respectively. Tumors were treated by intratumoral administration of MBTA, a formulation containing resiquimod, poly(I:C), LTA, anti-CD40 antibody, and mannan-BAM (a phagocytosis-stimulating mannan anchored to the tumor cell membrane via a biocompatible membrane anchor, BAM). Multiple variants of the therapy were tested, differing in composition and timing, including treatment of recurrences.</p><p><strong>Results: </strong>Intratumoral MBTA immunotherapy administered using an optimized 5 × 2 schedule resulted in an 87.5% survival rate in mice bearing subcutaneous Panc02 tumors. MBTA immunotherapy also effectively treated spontaneous local Panc02 recurrences that developed in a small subset of mice. High efficacy of MBTA was further confirmed in a murine model of colon adenocarcinoma.</p><p><strong>Conclusion: </strong>These findings suggest that MBTA is a promising therapeutic approach for primary and recurrent pancreatic adenocarcinoma, with potential for broader clinical application.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2683273"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13285565/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148275774","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":"STARD10 promotes progression of HER2+ breast cancer and intracellular lipid metabolism via the cAMP/PKA/CREB1 signaling axis.","authors":"Siyao Liu, Jing Gao, Yichen Niu, Xinnan Dong, Zhiming Zhang, Xiao Teng, Zhaorong Li, Siyan Zhang, Yong Meng, Ming-Qing Gao","doi":"10.1080/15384047.2026.2688544","DOIUrl":"10.1080/15384047.2026.2688544","url":null,"abstract":"<p><strong>Background: </strong>Although targeted therapies have improved clinical outcomes, HER2+ breast cancer remains a significant clinical challenge due to its aggressive behavior and unfavorable prognosis. Emerging evidence indicates that dysregulated lipid metabolism plays a critical role in tumorigenesis and metastasis, suggesting that targeting lipid metabolism may represent a promising therapeutic strategy. STARD10, a lipid transport protein, plays a pivotal role in regulating lipid metabolism. However, its function in mediating lipid metabolism and tumor progression in HER2+ breast cancer remains unclear.</p><p><strong>Methods: </strong>The expression level and prognostic relevance of STARD10 in HER2+ breast cancer were analyzed using public databases and clinical cohorts. CCK-8, EdU, colony formation, transwell, LD540, and Nile Red staining assays were performed in SKBR3 and HCC1954 cells. Subcutaneous implantation and tail vein injection were performed to evaluate the effects of STARD10 overexpression on tumor growth and lung metastasis in vivo. The mechanism was validated by RNA-seq and Western blotting.</p><p><strong>Results: </strong>STARD10 expression was upregulated in HER2+ breast cancer tissues and was significantly correlated with poor prognosis. Functionally, STARD10 overexpression enhanced HER2+ breast cancer cell proliferation, migration, invasion, and lipid droplets accumulation. Moreover, STARD10 overexpression markedly accelerated tumor growth and lung metastasis in vivo. Mechanistically, STARD10 was found to drive malignant phenotypes via activation of the cAMP/PKA/CREB1 signaling axis.</p><p><strong>Conclusion: </strong>STARD10 promotes malignant progression of HER2+ breast cancer and lipid droplets accumulation by activating the cAMP/PKA/CREB1 pathway. These findings suggest that STARD10 and the cAMP/PKA/CREB1 signaling axis as potential therapeutic targets for the treatment and prevention of HER2+ breast cancer.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2688544"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13274131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257395","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":"Statement of Retraction: Long noncoding RNA MALAT1 knockdown inhibits progression of anaplastic thyroid carcinoma by regulating miR-200a-3p/FOXA1.","authors":"","doi":"10.1080/15384047.2026.2746185","DOIUrl":"10.1080/15384047.2026.2746185","url":null,"abstract":"","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2746185"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13656804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134669","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":"ULK1's role in cancer progression and its emerging therapeutic potential.","authors":"Jack D Webb, Trevor G Shepherd","doi":"10.1080/15384047.2026.2680347","DOIUrl":"https://doi.org/10.1080/15384047.2026.2680347","url":null,"abstract":"<p><p>Macroautophagy (autophagy) enables cellular stress adaptation by degrading damaged components; ULK1, a serine/threonine kinase, initiates this process in response to nutrient and energy cues. While autophagy is well studied, few investigations have directly tested ULK1 in cancer progression. Emerging functional data across numerous cancers indicate that ULK1 can promote or restrain malignant behavior through both autophagy-dependent and autophagy-independent mechanisms, modulating mitochondrial quality, anoikis escape, invasion, therapy adaptation, and immune visibility. Pharmacology has advanced from early ULK1/2 inhibitors to structure-guided and machine learning-derived inhibitors with improved potency and selectivity. The first clinical agent, DCC-3116, demonstrates on-target engagement with acceptable tolerability and is being evaluated in combinations where therapy induces autophagy. Here, we review ULK1 as a regulator of cancer progression, synthesizing pan-cancer clinical and functional evidence alongside the evolving pharmacology of ULK1 modulation to define the settings in which its targeted inhibition may be most effectively translated.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2680347"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148270477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of STAT3-mediated glycolysis by bruceine D suppresses non-small-cell lung cancer progression <i>in vitro</i> and <i>in vivo</i>.","authors":"Yu Zhu, Xuan Xu, Xiaofan Hong, Jiayi Zhang, Yi Zhou, Aofeng Sun, Yihan Ye, Yini Xu, Huanhai Xu, Haiyang Zhao, Chengguang Zhao, Xing Jin, Lehe Yang, Jianxiao Zheng","doi":"10.1080/15384047.2026.2665867","DOIUrl":"10.1080/15384047.2026.2665867","url":null,"abstract":"<p><strong>Background: </strong>Non-small-cell lung cancer (NSCLC) is one of the deadliest malignancies in the world. Signal transducer and activator of transcription 3 (STAT3) plays an important role in the progression of NSCLC. Bruceine D is a bioactive quassinoid compound extracted from <i>Brucea javanica</i>, a plant widely used in traditional Chinese medicine.</p><p><strong>Methods: </strong>Tests of cell function were performed to observe the effects of bruceine D on human NSCLC cell lines (H460, PC-9, and SKMES-1). Levels of STAT3, phosphorylated STAT3, Survivin, and other apoptosis-related proteins were detected via Western blotting. The binding of bruceine D to STAT3 was examined using molecular dynamics simulations and surface plasmon resonance spectroscopy. The effect of bruceine D on STAT3 nuclear localization was examined by immunofluorescence. Furthermore, the glucose uptake, lactate production, and extracellular acidification rates of NSCLC cells were analyzed to confirm that bruceine D inhibited glycolysis in NSCLC. The efficacy of bruceine D <i>in vivo</i> was evaluated in a mouse xenotransplantation model.</p><p><strong>Results: </strong>Bruceine D significantly reduced the viability of NSCLC cells, promoted apoptosis, and inhibited the growth of tumors in a mouse xenograft model. Bruceine D was found to bind directly to STAT3, inhibiting glycolysis in NSCLC cells. Western blotting results suggested that the antitumor effects of bruceine D might be mediated by the inhibition of the phosphorylation and nuclear translocation of STAT3.</p><p><strong>Conclusion: </strong>Bruceine D exerts a strong inhibitory effect on NSCLC <i>in vitro</i> and <i>in vivo</i>. Bruceine D has potential application prospects in the field of anti-NSCLC therapy.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2665867"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13166240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834088","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":"Deguelin inhibits perineural invasion in esophageal squamous cell carcinoma via targeting BDNF/TrkB axis.","authors":"Qiying Wei, Liuyang Bai, Liangying Yan, Zhongyu Wang, Rongyao Jin, Bingjie Li, Wenbo Cao, Saijun Mo","doi":"10.1080/15384047.2026.2644788","DOIUrl":"10.1080/15384047.2026.2644788","url":null,"abstract":"<p><strong>Background: </strong>Perineural invasion (PNI) represents a uniquely distinctive pathway for tumor metastasis, but its underlying molecular mechanisms and therapy remain unclear.</p><p><strong>Methods: </strong>Bioinformatics analysis and transcriptomic sequencing were first employed to investigate the involvement of the BDNF/TrkB axis in the ESCC PNI, which was validated with ESCC cells co-cultured with a dorsal root ganglia system (ESCC/DRG model), a mouse PNI model, and ESCC tissues, mainly using microscopic imaging, IVIS Spectrum <i>in vivo</i> imaging, Western blot (WB), and immunohistochemistry (IHC). Additionally, transcriptomic sequencing and WB were conducted to analyze the downstream molecular mechanisms of the BDNF/TrkB axis. Similar experiments were applied to investigate the role of Deguelin in ESCC PNI. Deguelin's interaction with BDNF was assessed using computational docking, pull-down assays, cellular thermal shift assays, surface plasmon resonance (SPR) and WB. Its inhibitory effects on the ESCC PNI were further evaluated through rescue experiments, where BDNF overexpression was used to counteract Deguelin's activity.</p><p><strong>Results: </strong>The BDNF/TrkB axis is closely associated with the PNI in ESCC. This pathway plays a pivotal role in driving PNI progression via Akt signaling. Deguelin was identified as an effective inhibitor of PNI in ESCC. Mechanistically, BDNF was revealed to be a key binding target of Deguelin, which disrupts PNI development by modulating the BDNF/TrkB/Akt axis. Notably, overexpression of BDNF can counteract Deguelin's inhibitory effects on ESCC growth and PNI progression.</p><p><strong>Conclusion: </strong>The BDNF/TrkB axis promotes the progression of ESCC PNI, and Deguelin inhibits ESCC PNI by targeting this axis, enhancing the understanding of PNI's molecular mechanisms and offering new therapeutic options.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2644788"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147479944","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":"Centromere protein I promotes hepatocellular carcinoma progression by activating PI3K/AKT/mTOR-CDK2 cascade.","authors":"Demeng Liu, Peihao Yang, Jiyao Wang, Junle Li, Xin Wang, Xiaohui Gu, Chao Liu, Yan Fang","doi":"10.1080/15384047.2026.2667596","DOIUrl":"10.1080/15384047.2026.2667596","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is characterized by high recurrence rates and limited targeted therapies. Centromere protein I (CENPI), a core kinetochore component linked to chromosomal instability, is dysregulated in multiple malignancies, yet its role and mechanism in HCC progression remain incompletely elucidated.</p><p><strong>Methods: </strong>CENPI expression was quantified in paired human HCC tissues and orthotopic rat HCC models via immunohistochemistry (IHC) and western blot (WB). Gain- and loss-of-function assays were performed in HepG2 cells and validated in Hep3B cells to evaluate the effects of CENPI modulation on cell proliferation, migration, invasion, apoptosis, and cell cycle dynamics. Mechanistic analyses included pathway enrichment and WB, with validation via rapamycin in HepG2 cells and LY294002 in Hep3B cells. In vivo tumor growth and signaling alterations were assessed in orthotopic HCC models following CENPI silencing.</p><p><strong>Results: </strong>CENPI was upregulated in HCC tissues and orthotopic tumors, correlating with poor survival. CENPI depletion suppressed proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while enhancing apoptosis and inducing G1 arrest; overexpression was pro-oncogenic. Mechanistically, CENPI activated the PI3K/AKT/mTOR-CDK2 axis, upregulating CDK2, and modulating EMT markers. Rapamycin abrogated CENPI-induced oncogenic signaling in vitro, and CENPI silencing reduced in vivo tumor burden by 65% while suppressing the pathway and EMT.</p><p><strong>Conclusion: </strong>CENPI may function as an oncogenic regulator in HCC through activation of the PI3K/AKT/mTOR-CDK2 cascade, linking cell cycle progression to EMT-associated invasiveness. These findings provide a preclinical rationale for further evaluating CENPI and its related signaling axis as potential prognostic and therapeutic targets in broader HCC models and clinical cohorts.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2667596"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13174019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147926661","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":"Suppression of LncRNA AC008406.3 sensitizes breast cancer cells to docetaxel via triggering cuproptosis.","authors":"Chenguang Liu, Shiyang Liu, Zonghong Lu, Xinchen Cao, Xiaofei Tong, Ieong Sun, Jie Hao, Lin Zhang","doi":"10.1080/15384047.2026.2676474","DOIUrl":"10.1080/15384047.2026.2676474","url":null,"abstract":"<p><strong>Background: </strong>Docetaxel (DTX) is one of the commonly used chemotherapeutic agents for breast cancer. Cuproptosis, a newly defined form of cell death, significantly influences tumor progression. This study aims to identify cuproptosis-related long non-coding RNAs (lncRNAs) involved in regulating the sensitivity of breast cancer to DTX.</p><p><strong>Materials: </strong>Cuproptosis-related prognostic lncRNAs in breast cancer were identified through integrated co-expression, differential expression, and prognostic analyses based on the TCGA-BRCA cohort. The role of the identified lncRNA AC008406.3 in regulating cuproptosis in breast cancer cells was experimentally verified. The impact of DTX on the induction of cuproptosis was investigated, and rescue experiments were conducted to validate the involvement of AC008406.3 in modulating breast cancer sensitivity to DTX.</p><p><strong>Results: </strong>AC008406.3 was identified as a potential cuproptosis-related prognostic lncRNA in breast cancer, exhibiting high expression in breast cancer samples, which was associated with unfavorable prognostic outcomes. Knockdown of AC008406.3 specifically induced cuproptosis in breast cancer cells, as evidenced by increased intracellular copper levels and downregulation of lipoylated proteins and Fe-S cluster proteins, thereby suppressing cell proliferation, invasion, and migration; conversely, AC008406.3 overexpression elicited opposite phenotypic changes. Notably, DTX induced the occurrence of cuproptosis in breast cancer, whereas AC008406.3 suppressed this process, thereby diminishing DTX efficacy. However, AC008406.3 knockdown synergistically enhanced the anti-tumor efficacy of DTX in inhibiting breast cancer growth.</p><p><strong>Conclusion: </strong>AC008406.3 reduces the sensitivity of breast cancer to DTX by suppressing cuproptosis. Targeting AC008406.3 may represent a potential strategy to sensitize breast cancer cells to DTX.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2676474"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13215318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027214","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}