Cancer Cell International最新文献

{"title":"Hsa_circ_0059511 promote glioma cell proliferation and migration through hsa-miR-194-5p/HBEGF axis.","authors":"Yajun Jing, Huang-Cheng Shang-Guan, Jiawei Cai, Jinye Su, Wei Huang, Qiu He, Xiaoyong Chen, Dezhi Kang, Zanyi Wu","doi":"10.1186/s12935-025-03815-w","DOIUrl":"10.1186/s12935-025-03815-w","url":null,"abstract":"<p><p>A growing number of studies have highlighted the critical role that circular RNAs play in cancer. We previously observed that hsa_circ_0059511 was markedly upregulated in glioma tissues, suggesting that it may play an oncogenic role in gliomas. But its mechanism is not clear. The aim of the present study was to investigate the biological function of hsa_circ_0059511 in gliomas. First, the expression levels of heparin-binding EGF-like growth factor (HBEGF), hsa_circ_0059511, and hsa-miR-194-5p in glioma tissues and cells were measured by qRT-PCR. Furthermore, cell viability, migration, and invasion were evaluated in vitro using CCK8 assay, EdU assay, and Transwell invasion assay after pcNDA-hsa_circ_0059511 transfection to increase hsa_circ_0059511 and siRNA transfection to suppress hsa_circ_0059511 in glioma cells. Finally, RNA immunoprecipitation (RIP) and a dual-luciferase reporter assay were used to determine the association between hsa-miR-194-5p and hsa_circ_0059511 or HBEGF. Our results showed that the expression levels of hsa_circ_0059511 were significantly increased in glioma tissues and cells compared to the control group (all p < 0.05). Furthermore, cell proliferation and invasion in vitro were restricted by knockdown of hsa_circ_0059511. Of note, we found that downregulation of hsa-miR-194-5p, a target microRNA of hsa_circ_0059511, could reverse the reduction in glioma cell proliferation and migration caused by silencing of hsa_circ_0059511. At the same time, we also found that hsa-miR-194-5p could suppress the proliferation and migration of glioma cells by inhibiting the expression of HBEGF, a target gene of hsa-miR-194-5p. Overall, our results showed that hsa_circ_0059511 increased HBEGF expression by sponging hsa-miR-194-5p to promote tumor cell migration and proliferation.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"219"},"PeriodicalIF":5.3,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12181929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA H19 acts as a ceRNA to promote glioblastoma malignancy by sponging miR-19b-3p and upregulating SERPINE1.","authors":"Wonyi Jang, Mijung Im, Goeun Yoon, Jungwook Roh, Wanyeon Kim","doi":"10.1186/s12935-025-03868-x","DOIUrl":"10.1186/s12935-025-03868-x","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma (GBM) is a highly aggressive brain tumor, characterized by genetic complexity and resistance to treatment. Despite significant advancements in cancer research, the mechanisms driving GBM progression remain poorly understood. This study investigates the molecular pathways associated with GBM, and focuses on long non-coding RNA H19 and its role in tumor growth and progression.</p><p><strong>Methods: </strong>Analysis of Gene Expression Omnibus (GEO) dataset was performed to identify differentially expressed genes in GBM cells with H19 overexpression, revealing serpin family E member 1 (SERPINE1) as a potential target. Bioinformatics analyses were used to evaluate the differential expression of H19 and SERPINE1 in GBM tissues, perform survival analysis, and predict miR-19b-3p as a candidate miRNA. The expression levels of H19, miR-19b-3p, and SERPINE1 were validated using RT-qPCR and Western blotting. Dual-luciferase reporter assays were conducted to confirm the direct interactions between H19, miR-19b-3p, and SERPINE1. Cell viability and motility assays were performed to assess the effects of modulating H19/miR-19b-3p/SERPINE1 expression on cell survival, migration, and invasion.</p><p><strong>Results: </strong>Bioinformatics analyses identified SERPINE1 as an oncogene upregulated in GBM cells with H19 overexpression, and the overexpression of H19 and SERPINE1 was linked to poor prognosis in GBM patients. Experimental validation demonstrated that H19 upregulates SERPINE1 expression, while miR-19b-3p directly binds to both H19 and SERPINE1, suppressing SERPINE1 expression. Functional assays further confirmed that H19 promotes cell survival, migration, and invasion, whereas miR-19b-3p inhibits these processes by downregulating SERPINE1.</p><p><strong>Conclusions: </strong>These findings reveal a novel mechanism whereby H19 drives GBM progression by acting as a competing endogenous RNA (ceRNA) to sponge miR-19b-3p and upregulate SERPINE1 expression. Our results offer new insights into the regulatory interplay among H19, miR-19b-3p, and SERPINE1 in GBM cell lines, a relationship that has not been clearly defined in previous research. Moreover, the H19/miR-19b-3p/SERPINE1 axis highlights the potential use of H19, miR-19b-3p, and SERPINE1 as promising biomarkers and therapeutic targets in GBM.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"217"},"PeriodicalIF":5.3,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12177970/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cannabidiol (CBD) as a potential therapeutic agent for liver cancer: a comprehensive review of current evidence.","authors":"Mojtaba Esmaeli, Maryam Dehghanpour Dehabadi","doi":"10.1186/s12935-025-03870-3","DOIUrl":"10.1186/s12935-025-03870-3","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a major cause of cancer-related mortality with limited treatment options. Cannabidiol (CBD), a non-psychoactive compound from Cannabis sativa, has shown anticancer properties. This review analyzes CBD's therapeutic potential in HCC, focusing on mechanisms, preclinical/clinical findings, and integration into treatment strategies. A systematic search (PubMed, Scopus, Web of Science, Google Scholar) up to March 2025 identified 16 relevant studies (in vitro, in vivo, clinical). CBD exerts antitumor effects via multiple pathways, including apoptosis, autophagy regulation, metastasis suppression, and tumor microenvironment modulation. CBD interacts with the endocannabinoid system (ECS), inhibits oncogenic signaling (PI3K/AKT/mTOR), and enhances chemotherapeutic efficacy (sorafenib, cabozantinib). Studies show CBD induces pyroptosis via caspase-3/GSDME, and modulates autophagy by inhibiting the PI3K/Akt/mTOR pathway. It also sensitizes HCC cells to sorafenib and cabozantinib. Preclinical results are promising, but clinical studies are limited. Challenges like bioavailability and potential hepatotoxicity require investigation. Future research should optimize formulations, determine dosing, and conduct clinical trials to validate CBD's efficacy/safety in HCC patients. Validated CBD could offer an innovative HCC management option.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"215"},"PeriodicalIF":5.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12178001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive analysis reveals CLDN9 is a new biomarker in human cancers and immunotherapeutic target for glioblastoma multiforme.","authors":"Yuanyuan Zhu, Ning Li, Fang Peng","doi":"10.1186/s12935-025-03852-5","DOIUrl":"10.1186/s12935-025-03852-5","url":null,"abstract":"<p><strong>Background: </strong>Claudin-9 (CLDN9) plays a pivotal role in forming tight junctions and adhesion among epithelial cells. Despite its importance, comprehensive investigations into the role of CLDN9 in various cancers have been lacking.</p><p><strong>Methods: </strong>We conducted a thorough analysis of CLDN9 across multiple cancer types using omics data and assessed its expression in glioblastoma multiforme (GBM) tissues via immunohistochemistry. To explore the impact of CLDN9 on tumor growth, we employed a subcutaneous GBM animal model. Furthermore, we utilized transwell experiments to evaluate cell migration and invasion capabilities.</p><p><strong>Results: </strong>Our findings reveal significant variations in CLDN9 expression across different cancers and among molecular and immune subtypes. CLDN9 demonstrates impressive predictive accuracy for certain cancer types and shows strong associations with cancer prognosis. IHC confirmed downregulated CLDN9 expression in GBM tissues, and its expression correlated with clinicopathological parameters of GBM patients. Specifically, in GBM, CLDN9 expression negatively correlated with activated CD8 T cells, activated dendritic cells, plasmacytoid dendritic cells, and type 1 helper cells. Moreover, we observed associations between CLDN9 expression and immunostimulators, immunoinhibitors, and major histocompatibility complex molecules. In vitro experiments indicated that CLDN9 overexpression reduced the migratory and invasive capabilities of GBM cells.</p><p><strong>Conclusions: </strong>Overall, our study provides valuable insights into the role of CLDN9 in various tumors and lays a foundation for more precise and individualized immunotherapy approaches for GBM in the future.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"216"},"PeriodicalIF":5.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12178002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC00525 drives aggressive phenotypes in bladder cancer via YAP stabilization-mediated transcriptional activation.","authors":"Jiaming Liang, Shuyue Guo, Youzhi Wang, Qian Cao, Tao Guo, Diansheng Zhou, Junbo Li, Yihao Liao, Boqiang Zhong, Ning Jiang","doi":"10.1186/s12935-025-03851-6","DOIUrl":"10.1186/s12935-025-03851-6","url":null,"abstract":"<p><p>LINC00525, a long noncoding RNA (lncRNA), has been implicated in the regulation of cancer progression across various types. However, its role in bladder cancer (BLCA) remains unconfirmed. In this study, we observed upregulation of LINC00525 expression in both bladder cancer tissues and cell lines compared to normal controls. Among the 12 pairs of collected tissue samples, LINC00525 exhibited higher expression levels in muscle-invasive bladder cancer (MIBC) tissues than in non-muscle-invasive bladder cancer (NMIBC) tissues, indicating a positive correlation between LINC00525 levels and bladder cancer progression. In vitro experiments demonstrated that knockdown of LINC00525 significantly inhibited proliferation, migration, and invasion of bladder cancer cell lines; conversely, overexpression of LINC00525 had the opposite effect. Bioinformatic analysis revealed an association between LINC00525 and YAP, which was further confirmed by western blotting and PCR analysis using patient tissues. Mechanistically, we found that LINC00525 reduced phosphorylation of YAP at serine 127 (S127), promoting its nuclear import to exert transcriptional regulatory effects on target genes. Additionally, LINC00525 inhibited YAP ubiquitination by acting on YAP lysine 321 (K321), thereby increasing its stability to prevent degradation. Through in vivo and in vitro experiments, we demonstrated the YAP-mediated promoting effect of LINC00525 on bladder cancer cells and tumor growth. Our study reveals the involvement of the LINC00525/YAP axis in regulating bladder cancer development, suggesting a potential therapeutic strategy for malignant tumors characterized by high levels of LINC00525 expression.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"214"},"PeriodicalIF":5.3,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12172227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Migration and invasion of cancer stem cells are prevented by low-intensity pulsed ultrasound therapy.","authors":"Alba Calero, Tamara Fernández-Marcelo, Paulina Sury, Beatriz de Lucas, Beatriz G Gálvez","doi":"10.1186/s12935-025-03854-3","DOIUrl":"10.1186/s12935-025-03854-3","url":null,"abstract":"<p><strong>Background: </strong>Ultrasound is considered a safe and non-invasive tool in regenerative medicine. In particular, low-intensity pulsed ultrasound (LIPUS) has been used in the clinic for more than twenty years for applications in bone healing. It has been demonstrated to be an effective tool to treat different chronic diseases. We sought to evaluate the effects produced by LIPUS on the properties of human breast cancer stem cells (bCSCs).</p><p><strong>Methods: </strong>Cells were stimulated using a traditional ultrasound device with the following parameters: 0.05 W/cm² with 10% duty cycle, frequency of 3 MHz and 8 pulses.</p><p><strong>Results: </strong>At the parameters used, the ultrasound did not directly affect bCSC proliferation, with no evident changes in morphology. In contrast, the ultrasound protocol affected the migration and invasion ability of bCSCs, limiting their capacity to advance while a major affection was detected on their angiogenic properties. LIPUS-treated bCSCs were unable to transform into aggressive metastatic cancer cells, by decreasing their migration and invasion capacity as well as vessel formation. Finally, RNA-seq analysis revealed major changes in gene expression, with 676 differentially expressed genes after LIPUS stimulation, 578 upregulated and 98 downregulated.</p><p><strong>Conclusions: </strong>Overall, these results highlight the potential of LIPUS as a promising non-invasive therapy to target bCSCs and attenuate its capacity to drive migration, invasion, angiogenesis and, ultimately, tumor malignancy. Besides, the ability of LIPUS to modulate gene expression points out its capacity to broadly influence the cellular transcriptome. Therefore, the application of LIPUS as an antitumor therapeutic agent targeting bCSCs may offer a promising new approach to treat cancer. In vivo functional experiments will determine in the future the relevance of LIPUS application for the development of metastasis.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"212"},"PeriodicalIF":5.3,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12166576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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: Overexpression of LncRNA PIK3CD-AS1 promotes expression of LATS1 by competitive binding with microRNA-566 to inhibit the growth, invasion and metastasis of hepatocellular carcinoma cells.","authors":"Wei Song, Jingjing Zhang, Jianbo Zhang, Miaomiao Sun, Qingxin Xia","doi":"10.1186/s12935-025-03850-7","DOIUrl":"10.1186/s12935-025-03850-7","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"213"},"PeriodicalIF":5.3,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12166625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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 circadian-related prognostic signature highlights RBM17 as a stemness regulator in liver cancer.","authors":"Jingsong Yan, Xiao Yang, Jiabin Lu, Shasha Wu, Yanchen Wang, Yuyang Du, Jingyi Zheng, Fenfen Wang, Han Gao, Hui Yang, Shaoyan Xi, Yan Li","doi":"10.1186/s12935-025-03843-6","DOIUrl":"10.1186/s12935-025-03843-6","url":null,"abstract":"<p><p>The liver exhibits extensive circadian regulation among organs. Epidemiological studies have substantiated that disruptions in circadian rhythm constitute a risk factor for the oncogenesis of liver cancer. Nonetheless, the molecular underpinnings of how circadian dysregulation influences liver cancer progression remain elusive. Our research aims to elucidate these mechanisms and develop a predictive model for prognosis and treatment responsiveness. Our multi-omics analysis revealed extensive dysregulation of liver circadian genes (LCGs) in liver cancer. Employing machine learning algorithms, we pinpointed four pivotal dysregulated LCGs. Through the integration of single-cell, bulk, and spatial transcriptomics, we further elucidated the interconnections between LCGs dysregulation and the tumor microenvironment. In vivo and in vitro experiments demonstrated that RBM17, identified as a crucial dysregulated LCG, promotes the progression of liver cancer and cisplatin resistance by facilitating cancer stem cell phenotype. The circadian prognosis scores (CPS), based on these four genes, effectively reflected the prognosis of liver cancer patients and their responses to various therapeutic interventions. Mechanism of Action (MOA) analysis suggested that high CPS level may sensitize tumors to cell cycle-targeted therapies. Collectively, our findings provide new insights into the interplay between liver circadian gene regulation and liver cancer progression, and propose novel therapeutic targets for liver cancer.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"211"},"PeriodicalIF":5.3,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12166579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correspondence: Highlighting the importance of immune system changes induced by physical activity and green tea in cancer management.","authors":"Amirhossein Ahmadi Hekmatikar","doi":"10.1186/s12935-025-03842-7","DOIUrl":"10.1186/s12935-025-03842-7","url":null,"abstract":"<p><p>In recent years, researchers have increasingly emphasized the significance of exercise in cancer treatment from the perspective of exercise oncology. Additionally, there has been growing interest in the potential role of medicinal plants in cancer therapy. However, the term \"cancer treatment\" encompasses numerous critical considerations, among which immunological factors are particularly significant. A recent and noteworthy review by Liu et al. (2025) [1], titled The Interplay of Exercise and Green Tea: A New Road in Cancer Therapy, explored novel perspectives on the roles of exercise and green tea in cancer treatment. While their analysis provides valuable insights, it unfortunately overlooks the crucial aspect of immunological changes, instead focusing primarily on the mechanisms through which physical activity and green tea contribute to cancer therapy. Given the centrality of immunological responses in cancer treatment, it is essential to examine the immunological changes induced by exercise and green tea, as well as their potential interactions. The failure to address these immunological aspects represents a significant research gap. In this article, we aim to bridge this gap by highlighting the immunological changes associated with exercise and green tea, thereby contributing new perspectives to future studies in the field.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"210"},"PeriodicalIF":5.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12164108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of β3-adrenergic receptor agonist on tumor progression and metastasis in renal cell carcinoma models.","authors":"Jee Soo Park, Myung Eun Lee, Minsun Jung, Jongchan Kim, Won Sik Jang, Won Sik Ham","doi":"10.1186/s12935-025-03834-7","DOIUrl":"10.1186/s12935-025-03834-7","url":null,"abstract":"<p><strong>Background: </strong>β3-adrenergic receptor (β3-AR) agonists, widely used in clinical urology, have recently been implicated in modulating cancer progression. While prior studies have reported both pro- and anti-tumor effects via fat browning and immune modulation, the mechanisms and organ-specific outcomes remain unclear. We aimed to confirm the effects of β3-AR agonists on primary tumors and lung metastasis using metastatic orthotopic murine renal cell carcinoma (RCC) models.</p><p><strong>Methods: </strong>Metastatic orthoptic murine RCC models were developed, and mirabegron, a β3-AR agonist, was orally administered at different dosages and exposure times. The mice were later sacrificed and their kidney and lung tissues harvested. The primary tumor weight and lung nodule number were noted. Perirenal adipose tissue (PAT) browning and tumor immune microenvironment (TIME) remodeling were evaluated and compared between the mirabegron and vehicle treatment groups.</p><p><strong>Results: </strong>Mirabegron-treated mice showed a significant increase in tumor growth in the early phase; however, tumor growth rates reduced (by > 56%) in the mid and late phases. Mirabegron significantly increased the lung metastatic burden (by > 41%) in all phases. Mirabegron modulated TIME both in primary tumors and lung nodules and increased PAT browning.</p><p><strong>Conclusions: </strong>The β3-AR agonist increases PAT browning, initially promoting primary tumor progression and possibly contributing to tumor initiation, but eventually inducing immune tolerance, leading to anticancer effects on primary tumors. Effects on lung metastases differed from those on primary tumors.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"209"},"PeriodicalIF":5.3,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12153155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}