Journal of Experimental & Clinical Cancer Research最新文献

{"title":"Low-dose docetaxel reprograms CAR T cells for enhanced solid tumor immunity.","authors":"Songshan Zhu, Jun Yin, Xin Fu, Weiqiang Yang, Yiwei Zeng, Rui Chen, Na Huang, Ling Zhang, Cong Yu, Qianying Huang, Ping Ouyang, Kaisong Huang, Hangjiu Su, Dan Jiang, Guangxian Xu","doi":"10.1186/s13046-026-03781-9","DOIUrl":"10.1186/s13046-026-03781-9","url":null,"abstract":"<p><strong>Background: </strong>Chimeric antigen receptor (CAR) T cell therapy in solid tumors is hampered by dense stromal barriers, rapid functional exhaustion, and limited persistence. Here, we report that low-dose docetaxel acts as an immunomodulatory primer that reprograms CAR T cells to address these barriers. Retrospective analysis of breast cancer patients identifies host lymphocyte reserve as a key determinant of docetaxel treatment benefit, implying an immunological component beyond direct tumor cell killing.</p><p><strong>Methods: </strong>Sub-cytotoxic docetaxel concentrations were evaluated in primary human T cells and CAR T cells using phenotypic, transcriptional, and functional assays. Secretory profiles and extracellular vesicle cargo were characterized, with efficacy assessed in 3D spheroids and xenograft models.</p><p><strong>Results: </strong>Docetaxel priming induces a \"Metabolic-Cycle Uncoupling\" state, constraining proliferation while enhancing cytotoxic effector potency and memory traits. This reprogramming is associated with upregulation of Rab27-dependent exosome biogenesis, accompanied by shedding of exhaustion markers (PD-1, CD57) and enrichment of cytotoxic ligands (FasL, TRAIL), CAR, and homing receptors (CCR5/CCR7). Primed CAR T cells exhibit improved antitumor efficacy with associated stromal remodeling and host T cell activation; secreted exosomes contribute to bystander tumor cell killing.</p><p><strong>Conclusions: </strong>These findings describe a non-genetic pharmacologic priming strategy with potential scalability and compatibility with existing manufacturing processes. This approach demonstrates enhanced CAR T cell performance against solid tumor barriers in preclinical models, highlighting the potential of chemotherapy-immunotherapy synergies.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13584523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148457585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selenite modulates phenotype-dependent epithelial-mesenchymal plasticity in pancreatic ductal adenocarcinoma: integrated in vitro analyses and patient-derived ex vivo tissue-slice cultures.","authors":"Ozan Aricak, Wenyang Shi, Carlos Fernández Moro, Mehran Ghaderi, Joakim Dillner, Jonas Fuxe, Mikael Björnstedt, Tímea Szekerczés","doi":"10.1186/s13046-026-03778-4","DOIUrl":"10.1186/s13046-026-03778-4","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic ductal adenocarcinoma (PDAC) is characterized by profound therapy resistance, desmoplasia, and phenotypic plasticity. While sodium selenite is a redox-active compound with reported tumor-selective cytotoxicity, its impact on epithelial-mesenchymal transition (EMT) states in PDAC remains insufficiently defined. We investigated whether selenite modulates EMT-associated phenotypes in a dose- and context-dependent manner using complementary in vitro and patient-derived ex vivo models and linked marker shifts to histological tumor regression in PDAC tissue slices.</p><p><strong>Methods: </strong>Three PDAC cell lines spanning distinct baseline EMT states (PANC-1, HPAF-II, Capan-2) were profiled by quantitative immunofluorescence for a predefined epithelial (EpCAM, cytokeratin, E-cadherin) and mesenchymal-associated (AHNAK2, ITGAV, vimentin) protein panel, with or without TGF-β pretreatment. Ex vivo tissue slices from treatment-naïve, non-metastatic PDAC resections (n = 10) were cultured in a within-patient paired design (0 h, 24 h, 48 h controls; 5 or 15 µM selenite during the second 24 h). Histological tumor regression was scored by a blinded pancreatic pathologist (Evans; CAP), compartment-resolved marker expression was quantified by multiplex immunofluorescence, and paired RNA sequencing was performed in a subset of donors (n = 4).</p><p><strong>Results: </strong>In vitro, responses were phenotype-contingent: the epithelial-biased HPAF-II and Capan-2 lines showed partial epithelial reinforcement and a consistent reduction of mesenchymal markers (particularly ITGAV, vimentin), whereas the mesenchymal-biased PANC-1 exhibited limited modulation. TGF-β pretreatment attenuated epithelial-promoting effects while suppression of mesenchymal markers was retained in a cell line-dependent manner. In ex vivo slices, selenite induced a dose-dependent improvement in histological tumor regression and increased the tumor-compartment epithelial-mesenchymal ratio at 15 µM, driven mainly by epithelial-marker upregulation, while mesenchymal markers showed no uniform suppression. At 15 µM, transcriptomics revealed a compact treatment response characterized by downregulation of basement-membrane/ECM modules without broad reversal across EMT gene sets; EMT scoring indicated heterogeneous shifts at 5 µM and a more consistent epithelial-leaning shift at 15 µM in most donors.</p><p><strong>Conclusions: </strong>Selenite was associated with reinforcement of epithelial features mainly in malignant PDAC compartments in a baseline-state-, dose-, and context-dependent manner, with higher-dose phenotypic shifts occurring alongside stronger histological tumor response in clinically proximal models.</p><p><strong>Trial registration: </strong>Not applicable.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"45 1","pages":""},"PeriodicalIF":14.3,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13366627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148438738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Long noncoding RNA lncTCF7, induced by IL-6/STAT3 transactivation, promotes hepatocellular carcinoma aggressiveness through epithelial-mesenchymal transition.","authors":"Jun Wu, Jun Zhang, Bin Shen, Kai Yin, Jianwei Xu, Wencan Gao, Lihong Zhang","doi":"10.1186/s13046-026-03777-5","DOIUrl":"10.1186/s13046-026-03777-5","url":null,"abstract":"","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"45 1","pages":""},"PeriodicalIF":14.3,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13355335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148425884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal stem cell-induced metabolic reprogramming of EGFR-wild-type tumor cells drives therapeutic resistance in EGFR-mutant non-small cell lung cancer.","authors":"Hongyu Bie, Jiarui Li, Jialin Liu, Jian Zhou, Tierun Wang, Xu Guo, Jiawei Liu, Yi You, Hui Huang, Shijia Li, Wanqiao Li, Xiubao Ren, Meng Wang, Wencheng Zhang, Cihui Yan","doi":"10.1186/s13046-026-03748-w","DOIUrl":"10.1186/s13046-026-03748-w","url":null,"abstract":"<p><strong>Background: </strong>To explore mesenchymal stem cell (MSC)-driven metabolic reprogramming of EGFR-wild-type (EGFR-wt) tumor cells contributing to tyrosine kinase inhibitor (TKI) resistance in EGFR-mutant (EGFR-mt) non-small cell lung cancer.</p><p><strong>Methods: </strong>Isolate MSCs from paired tumor and non-tumor lungs of EGFR-mt and EGFR-wt patients. Integrate transcriptional RNA sequencing, targeted free fatty acid and energy metabolomics to characterize signaling pathways promoting MSC-EGFR-wt tumor cell interaction within EGFR-mt tumors. Assess spatial correlation between these cells in TKI-resistant and TKI-sensitive patients using immunohistochemistry and multiplex immunofluorescence.</p><p><strong>Results: </strong>EGFR-mt lung cancer-derived MSCs (mtLC-MSCs) promoted EGFR-wt tumor proliferation, and reduced TKI efficacy in vivo. Mechanistically, mtLC-MSCs increased fatty acid levels, supporting stem-like features in EGFR-wt tumor cells. These effects were mediated by IL-6 and IL-1α secreted from mtLC-MSCs, which enhanced S100A9 expression in EGFR-wt tumor cells and activated downstream c-Myc/β-catenin-FASN signaling, driving fatty acid synthesis. TKI plus IL-6 pathway blockade reversed resistance in mice. In EGFR-mt NSCLC patients, the proportions mtLC-MSCs was comparable with mtTF-MSCs. TKI-resistant samples exhibited greater mtLC-MSCs wrapping density around tumor masses than sensitive samples. EGFR-mt tumor cells showed closer spatial proximity to mtLC-MSCs than did EGFR-wt cells.</p><p><strong>Conclusion: </strong>These findings firstly reveal the spatial heterogeneity and metabolic reprograming of EGFR-wt tumor cells driven by mtLC-MSCs in EGFR-mt tumors, providing novel insight into therapeutic resistance and potential combination strategies for TKI-resistant patients.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148425808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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 the myofibroblastic cancer-associated fibroblast phenotype to enhance anti-PD-1 response.","authors":"Katherine A Johnson, Anna E L Lippert, Alec Cornelio, Yousef Gadalla, Xingqi Shen, Sean G Kraus, Philip B Emmerich, Anna M Field, Alyssa K Steimle, Cheri A Pasch, Huy Q Dinh, Wei Zhang, Kristina A Matkowskyj, Dustin A Deming","doi":"10.1186/s13046-026-03779-3","DOIUrl":"10.1186/s13046-026-03779-3","url":null,"abstract":"<p><strong>Background: </strong>Cancer-associated fibroblasts (CAFs) are key modulators of tumor growth, the tumor immune context, and treatment response. CAFs take on diverse phenotypes with distinct functions. Myofibroblastic CAFs (myCAFs) regulate extracellular matrix remodeling, while inflammatory CAFs (iCAFs) modulate immune infiltration. Further studies are required to validate biomarkers of CAF phenotypes and to identify means to therapeutically manipulate CAFs.</p><p><strong>Methods: </strong>Single-cell RNA sequencing analysis was used to identify markers of CAF phenotypes in CRC. CAF markers were validated and compared to clinical characteristics using patient-derived CAF cultures, fixed human CRC samples, and publicly available RNA sequencing data. Therapeutics were prioritized for their potential to inhibit the myCAF phenotype and nilotinib was selected for validation in patient-derived CAFs. Overall changes in CAFs were evaluated via RNA-seq, and results validated with in vitro experiments. Finally, the feasibility of altering CAF phenotypes to affect treatment response was evaluated in vivo.</p><p><strong>Results: </strong>Here we identify disease-specific markers of colorectal CAFs that are functionally distinct, biologically identifiable, correlate with clinically relevant markers of disease, and can be therapeutically altered in vivo. High stromal expression of myCAF markers correlated with reduced infiltration of CD8⁺ T lymphocytes into the epithelial compartment compared to tumors with high stromal expression of iCAF markers. Nilotinib treatment inhibited myogenesis regulators myocardin and myocardin-related transcription factor A, which correlated with reduced expression of myCAF markers and extracellular matrix proteins and decreased tumor size in colorectal cancer-bearing mice when combined with anti-PD-1 therapy. We also identified PD-1 as a potential molecule that activates myocardin and myCAF expression, indicating a potential mechanism for increased response to the combination with anti-PD-1 therapy.</p><p><strong>Conclusions: </strong>These results highlight the feasibility of targeting CAF functions to improve therapeutic response, and support the investigation of nilotinib and anti-PD-1 therapy clinically.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13640252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148425853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicle-mediated GALNT1/RPRD1A glycosylation axis drives immune escape and peritoneal metastasis in gastric cancer.","authors":"Guohua Jin, Jianguang Zhang, Qingying He, Shiyu Chang, Zheyu Dong, Yang Shi","doi":"10.1186/s13046-026-03759-7","DOIUrl":"10.1186/s13046-026-03759-7","url":null,"abstract":"<p><strong>Background: </strong>Peritoneal metastasis represents one of the most lethal clinical manifestations of gastric cancer (GC) and is closely associated with immune evasion. Extracellular vesicles (EVs) have emerged as critical mediators of tumor-immune communication; however, the molecular mechanisms by which EV-associated glycosylation regulates immune escape and metastatic dissemination remain largely undefined.</p><p><strong>Methods: </strong>EVs derived from highly metastatic GC cells were isolated and functionally characterized in vitro and in humanized immune system mouse models. Their clinical relevance was evaluated using paired human GC specimens. Underlying mechanisms were investigated through genetic manipulation, lectin-based glycosylation assays, and immune cell co-culture experiments.</p><p><strong>Results: </strong>We identified GALNT1 as an EV-enriched glycosyltransferase that promotes GC cell invasion and suppresses CD8⁺ T-cell activation. Mechanistically, GALNT1-dependent O-GalNAc glycosylation of RPRD1A was associated with increased RPRD1A protein abundance without altering its mRNA expression. Increased RPRD1A acted as a key downstream effector driving immune escape and peritoneal metastasis. Clinically, GALNT1 and RPRD1A were significantly upregulated in GC tissues, positively correlated with each other, associated with reduced T-cell infiltration, and predictive of poor prognosis. In humanized mouse models, EV-mediated transfer of GALNT1 accelerated peritoneal dissemination and impaired antitumor immunity, whereas disruption of the GALNT1/RPRD1A axis restored T-cell infiltration and suppressed metastatic progression.</p><p><strong>Conclusions: </strong>These findings identify an EV-driven GALNT1/RPRD1A glycosylation axis as a previously unrecognized mechanism underlying immune escape and peritoneal metastasis in GC and support this pathway as a potential therapeutic target for advanced disease.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148377469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Nanovaccines with ferroptosis, necroptosis and STING-activation for synergistic immunotherapy.","authors":"Jia-Rui Du, Mu-Le Tu, Yong-Xu Xia, Yuan-Qiang Lin, Rui Yang, Chang Weng, Yi Liu, Hao Zhang, Hui Wang, Wen-Jie Feng, Deng-Ke Teng","doi":"10.1186/s13046-026-03770-y","DOIUrl":"10.1186/s13046-026-03770-y","url":null,"abstract":"","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"45 1","pages":""},"PeriodicalIF":14.3,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148370645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NHE7-Driven endoplasmic reticulum stress signaling transmission promotes malignant progression of endometrial cancer via c-Fos/PRSS1/ERP27 axis.","authors":"Shizhou Yang, Yuejiang Ma, Zhengyun Chen, Tingting Wu, Xiufeng Huang","doi":"10.1186/s13046-026-03773-9","DOIUrl":"10.1186/s13046-026-03773-9","url":null,"abstract":"<p><strong>Background: </strong>Endometrial cancer (EC) threatens women's health. The Na⁺/H⁺ Exchanger 7 (NHE7) is implicated in cancer progression, but its role in EC and potential link to endoplasmic reticulum (ER) stress remain poorly understood.</p><p><strong>Methods: </strong>NHE7 was overexpressed or knocked down in EC cells. Functional assays and transcriptomic analyses were performed. Supernatant (SN) or exosomes from donor EC cells were applied to recipient cells. Mechanistic studies included exosome inhibition (GW4869), bioinformatic analysis, dual-luciferase reporter assays, chromatin immunoprecipitation (ChIP), and ER stress manipulation (4-PBA/Tunicamycin). In vivo tumor models validated findings.</p><p><strong>Results: </strong>NHE7 promoted malignant phenotypes, EMT, and stemness via ER stress activation. SN/exosomes from NHE7-overexpressing cells transmitted these phenotypes and ER stress to recipient cells, which were blocked by GW4869 or 4-PBA. PRSS1 was identified as a key NHE7 downstream target, and its exosomal delivery mediated ER stress transmission. Mechanistically, NHE7 drove PRSS1 transcription in donor cells via ER stress-dependent c-Fos recruitment to the PRSS1 promoter. In recipient cells, PRSS1 upregulated ERP27 to amplify ER stress. TCGA data showed that high PRSS1 expression correlated with poor prognosis. In vivo, NHE7 accelerated tumor growth and upregulated PRSS1/ERP27, effects reversed by 4-PBA.</p><p><strong>Conclusion: </strong>NHE7 functions as a key regulator of ER stress signaling transmission in EC cells, driving malignant phenotypes and stemness through the c-Fos/PRSS1/ERP27 axis. Targeting this axis may offer a novel therapeutic strategy for EC.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13595798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148370641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adipocyte-rich microenvironment promotes TNBC progression through SIRT6-associated ACSL5 dysregulation and lipid storage-associated phenotypes.","authors":"Yingnan Li, Xinyi Sun, Jing Peng, Teng Ma, Changgen Liu, Haibo Wang","doi":"10.1186/s13046-026-03769-5","DOIUrl":"10.1186/s13046-026-03769-5","url":null,"abstract":"<p><strong>Background: </strong>Triple-negative breast cancer (TNBC) is highly aggressive and has strong metastatic potential, and effective targeted therapies remain limited. There is growing evidence that the adipocyte microenvironment plays an important role in tumor progression, but its specific mechanism remains to be studied. As a key enzyme for the activation of long-chain fatty acids, the role and regulatory mechanism of ACSL5 in TNBC have not been clarified.</p><p><strong>Methods: </strong>ACSL5 expression and clinical relevance were assessed using public datasets, clinical specimens, and TNBC cell models. The effect of ACSL5 knockdown and overexpression on the malignant phenotype of TNBC cells were evaluated. An adipocyte-TNBC co-culture system, PA/OA treatment, SIRT6 manipulation, co-immunoprecipitation, pan-acetylation assays, and ACSL5 K212/213 mutant analysis were used to investigate the SIRT6-ACSL5 regulatory mechanism. Lipid-associated phenotypes were examined by Oil Red O staining, TG measurement, FASN/CPT1A detection, and Seahorse analysis. In vivo validation was performed using an orthotopic mammary fat pad model in female NOD/SCID mice.</p><p><strong>Results: </strong>ACSL5 expression was reduced in TNBC tissues and cell lines, and lower ACSL5 expression was associated with aggressive disease features. Functionally, ACSL5 knockdown promoted TNBC cell viability, colony formation, migration, invasion, and EMT-associated changes, whereas ACSL5 overexpression exerted opposite effects. Adipocyte co-culture and PA exposure induced SIRT6 upregulation and ACSL5 downregulation, while SIRT6 knockdown partially restored ACSL5 expression. Mechanistically, SIRT6 interacted with ACSL5 and regulated ACSL5 pan-acetylation. Mutagenesis of a candidate K212/213-containing lysine motif suggested that this region may contribute to ACSL5 acetylation-associated functional regulation. Adipocyte co-culture and SIRT6 overexpression increased lipid droplet accumulation, intracellular TG storage, FASN expression, and EMT-associated changes, while reducing CPT1A expression. ACSL5 restoration partially reversed these lipid storage-associated malignant phenotypes. In an orthotopic mammary fat pad model using female NOD/SCID mice, ACSL5 overexpression suppressed tumor growth, lung metastatic involvement, Ki67 expression, tumor TG accumulation, and lipid metabolism-related marker changes, whereas ACSL5 knockdown produced the opposite effects.</p><p><strong>Conclusion: </strong>These findings suggest that adipocyte-derived fatty-acid cues may promote TNBC progression partly through SIRT6-associated ACSL5 dysregulation and lipid storage-associated phenotypic changes, highlighting ACSL5 as a potential lipid-related regulatory node in adipocyte-driven TNBC progression.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13579850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148370602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Copy number amplification-induced overexpression of lncRNA LOC101927668 facilitates colorectal cancer progression by recruiting hnRNPD to disrupt RBM47/p53/p21 signaling.","authors":"Zaozao Wang, Haibo Han, Chenghai Zhang, Chenxin Wu, Jiabo Di, Pu Xing, Xiaowen Qiao, Kai Weng, Hao Hao, Xinying Yang, Yifan Hou, Beihai Jiang, Xiangqian Su","doi":"10.1186/s13046-026-03772-w","DOIUrl":"10.1186/s13046-026-03772-w","url":null,"abstract":"","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"45 1","pages":""},"PeriodicalIF":14.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13321748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148363405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}