Molecular Cancer最新文献

{"title":"CircZFR/YTHDF3 axis drives lymph node metastasis in cervical cancer via FASN translation","authors":"Mingyi Zhou, Yan Gao, Yong Zhang, Lian He, Bo Gao, Yue Zhang, Francois X. Claret, George A. Calin, Danbo Wang","doi":"10.1186/s12943-025-02424-5","DOIUrl":"https://doi.org/10.1186/s12943-025-02424-5","url":null,"abstract":"Lymph node metastasis is a key driver of poor outcomes in cervical cancer. However, the molecular mechanisms of circular RNAs (circRNAs) driving cervical cancer lymph node metastasis remain unclear. We identified circZFR, fatty acid synthase (FASN) and YTH N6-methyladenosine RNA binding protein F3 (YTHDF3) protein expression in the cervical cancer patients with long and short disease-free survival (DFS). Functional experiments were performed to investigate the function of circZFR, FASN and YTHDF3 on cell migration and invasion. MeRIP-qPCR, RNA pulldown, RNA Immunoprecipitation (RIP), and Co-Immunoprecipitation (Co-IP) assays were executed to investigate the mechanism of circZFR regulating FASN protein expression. Our study reveals that elevated FASN protein is closely linked to metastasis and reduced survival, and identified a regulatory mechanism involving circular RNAs. We identified circZFR as a crucial regulator, significantly enhancing FASN protein expression. CircZFR overexpression was significantly correlated with accelerated lymph node metastasis and shortened DFS. Mechanistically, circZFR binds to the m6A reader protein YTHDF3, facilitating m6A recognition on FASN mRNA and recruiting the translation initiator eIF4A3, thereby boosting FASN translation. These findings establish circZFR as a pivotal driver of cervical cancer progression and highlight its inhibition as a promising therapeutic strategy.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"94 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144899157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Jab1 regulates HRR mRNA stability to modulate PARP inhibitor sensitivity in triple-negative breast cancer","authors":"Xin Peng, Yingying Wang, Zixiang Yu, Shengfan Huang, Shaolu Zhang, Zhenxing Zhong, Yongzhe Wang, Shanshan Liu, Kailin Wang, Christophe Nicot, Francois X. Claret, Dexin Kong","doi":"10.1186/s12943-025-02422-7","DOIUrl":"https://doi.org/10.1186/s12943-025-02422-7","url":null,"abstract":"Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype associated with the highest mortality rate among all breast cancer subtypes, primarily due to the absence of actionable therapeutic targets. Although poly (ADP-ribose) polymerase inhibitors (PARPi) have shown promising therapeutic effects in TNBC patients harboring homologous recombination deficiency (HRD), their clinical benefit remains limited, highlighting an urgent need for novel targets that enhance PARPi efficacy. This study investigates the role of Jab1 in regulating the stability of homologous recombination repair (HRR)-related RNAs and evaluates its potential as a therapeutic target to enhance PARPi sensitivity in TNBC. RNA-Seq analysis revealed that shRNA-mediated Jab1 knockdown profoundly affected HRR and DNA replication processes in TNBC cells. Using Nuclear Run-On Assay, RNA Immunoprecipitation, RNA Pull-Down Assay, and RIP-Seq, we identified Jab1 as a potential RNA-binding protein (RBP) that stabilizes HRR-related mRNAs by competing with the exosome complex. Genetic and pharmacological inhibition of Jab1 (using CSN5i-3) were evaluated for their impact on HRR efficiency, ionizing radiation (IR) sensitivity, and PARPi sensitivity. A comprehensive panel of in vitro assays was performed, including clonogenic survival assays, PrestoBlue assays, apoptosis assays, DR-GFP reporter assays, qRT-PCR, Western blot, comet assays, and immunofluorescence. In vivo efficacy was assessed using zebrafish xenografts, nude mouse xenografts, and syngeneic orthotopic mouse models to examine the therapeutic effect of Jab1 inhibition in combination with PARPi. Jab1 was found to be overexpressed in TNBC and correlated with poor clinical outcomes. Functional analyses revealed that Jab1 knockdown impaired HRR, increased DNA damage accumulation, and sensitized TNBC cells to IR and PARPi, irrespective of BRCA mutation status. Mechanistically, Jab1 functioned as an RBP through its MPN domain, stabilizing HRR-related transcripts by competitively antagonizing the RNA exosome complex. Pharmacological inhibition of Jab1 using CSN5i-3 recapitulated these effects and synergized with PARPi to induce synthetic lethality. In multiple preclinical models, this combination significantly suppressed tumor growth and promoted apoptosis. This study uncovers a novel role for Jab1 as an RBP, specifically through interactions between its MPN domain and HRR-related RNAs, regulating RNA stability and maintaining HRR competency. Targeting Jab1 represents a promising strategy to pharmacologically induce HRD and enhance the efficacy of PARPi therapies in TNBC. This combination approach may hold translational value for improving clinical outcomes in patients with TNBC.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"24 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144860093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurotransmitters: an emerging target for therapeutic resistance to tumor immune checkpoint inhibitors","authors":"Jiyuan Yang, Yu Wu, Xinhui Lv, Sicong Liu, Ziwen Yuan, Yafang Chen, Xiangyu Ding, Zhong Li, Xudong Wang","doi":"10.1186/s12943-025-02413-8","DOIUrl":"https://doi.org/10.1186/s12943-025-02413-8","url":null,"abstract":"The critical role of neurotransmitters in the resistance to tumor immune checkpoint inhibitor (ICI) is becoming increasingly significant in therapeutic contexts. ICIs work by enhancing antitumor immunity through the blockade of the PD-1/PD-L1 and CTLA-4 pathways. However, only 20% of patients experience durable efficacy, and the challenge of drug resistance limits the clinical application of these therapies. Drug resistance is closely linked to various factors within the tumor microenvironment, including the distribution of tumor-infiltrating lymphocytes, the function of tumor-associated macrophages, low expression levels of PD-L1, variations in tumor mutational burden, dysregulation of antigen presentation, and both genetic and epigenetic changes in tumor cells. In recent years, the importance of the neural-immune axis has gained attention. Abnormal nerve fiber growth or irregular secretion of neurotransmitters can contribute to immune evasion. Neurotransmitters such as dopamine, norepinephrine, and serotonin influence the tumor microenvironment by regulating the expression of immune checkpoints and the function of immune cells, which can promote immune escape. As a result, therapeutic strategies that target neurotransmitters and their receptors hold promise for overcoming resistance to ICIs. These strategies may significantly enhance the efficacy of ICIs and pave the way for new approaches in cancer therapy. This article reviews the relevant mechanisms and proposes potential therapeutic strategies, offering new insights for the field.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"290 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144819154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating neuroscience and oncology: neuroimmune crosstalk in the initiation and progression of digestive system tumors","authors":"Haonan Sun, Tao Wang, Xiangyan Jiang, Mingdou Li, Xiaoe He, Yong Ma, Xiangkai Li, Weilin Jin, Zuoyi Jiao","doi":"10.1186/s12943-025-02412-9","DOIUrl":"https://doi.org/10.1186/s12943-025-02412-9","url":null,"abstract":"Recent global data show that cancers of the digestive system are responsible for approximately one-third of all cancer-related deaths worldwide, underscoring the urgent need for innovative therapeutic strategies. In this context, emerging findings from neuroscience may unveil new avenues for tackling this pressing clinical problem. Over the past few years, rapid progress in cancer neuroscience has increasingly underscored the contribution of the nervous system to the development and progression of digestive tract tumors. Research has shown that the specialized neural network of the gastrointestinal tract establishes a framework for reciprocal interactions with digestive tract tumors. On this anatomical foundation, our review delves into the functional significance of these interactions, emphasizing the bidirectional regulatory pathways between the nervous system and tumor cells during disease progression and highlighting their intricate crosstalk with the immune microenvironment. In particular, it maps the molecular pathways by which both the central and peripheral nervous systems (PNS) modulate tumor initiation and progression. Moreover, it explains how neurotransmitters and neuroendocrine mediators drive tumor expansion through the activation of canonical oncogenic signaling cascades and the remodeling of the immunosuppressive microenvironment. This review seeks to elucidate the molecular underpinnings of neuro-immune-tumor crosstalk and to synthesize the latest neural-targeted therapeutic approaches. It also examines the principal obstacles that are impeding the clinical implementation of these interventions. By presenting an integrated overview, this work serves as a robust resource to inform future studies on neurobiological mechanisms and the development of novel therapies for gastrointestinal malignancies.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"16 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircRNA aptamer targets IGF2BP2 to overcome acquired BETi resistance","authors":"Christophe Nicot","doi":"10.1186/s12943-025-02423-6","DOIUrl":"https://doi.org/10.1186/s12943-025-02423-6","url":null,"abstract":"<p>Bromodomain-and-extra-terminal-domain (BET) proteins are critical epigenetic readers that recognize acetylated histones to regulate transcription activation [1]. Their crucial role in activating oncogene expression (particularly c-MYC) has positioned BET inhibitors (BETi) as promising epigenetic therapeutics for refractory malignancies, including triple-negative breast cancer (TNBC). However, the clinical efficacy of BETi has been substantially limited by the rapid emergence of drug resistance, evidenced by the termination of approximately 50% of BETi monotherapy trials for solid tumors [2]. This therapeutic challenge underscores the urgent need for innovative strategies to overcome BETi resistance. A recent breakthrough study by Guo et al. identified a circular RNA (circRNA) named BISC that overcomes acquired BETi resistance by specifically targeting the RNA-binding protein IGF2BP2 to suppress <i>c-MYC</i> mRNA translation [3]. These findings not only reveal a novel BETi resistance mechanism but also highlight the potential of circRNA-based therapies to address the critical challenge of drug resistance in TNBC.</p><p>Drug resistance represents a major limitation, primarily emerging through either target-specific modification (e.g. altered target expression or resistance-conferring mutations) or the compensatory activation of alternative survival pathways. This challenge is particularly pronounced for epigenetic inhibitors like BETi, where genome-wide transcriptional reprogramming can simultaneously activate both therapeutic and resistance pathways. In prostate cancer, intrinsic BETi resistance stems from ubiquitin system dysregulation, characterized by diminished SPOP-mediated degradation [4] or enhanced DUB3-mediated stabilization of BET proteins [5]. Similarly, non-small cell lung cancer (NSCLC) exhibits BETi resistance in <i>LKB1</i>-deficient specimens [6] or through BCL6/mTOR pathway activation following BRD3 inhibition [7]. Although <i>c-myc</i> functions as a primary BRD4 effector in BETi-sensitive malignancies such as TNBC [8] and acute myeloid leukemia (AML) [9], its reactivation following prolonged BETi exposure drives acquired drug resistance. Notably, Guo et al. recently identified a novel resistance mechanism in TNBC, where IGF2BP2-mediated translational control sustains c-MYC expression independent of transcriptional regulation (through β-catenin, GLI2, or MED1 activation) or protein stability [3] (Fig. 1). These findings reveal enhanced c-MYC translation as a previously underappreciated cause of epigenetic therapy resistance.</p><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 1</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02423-6/MediaObjects/12943_2025_2423_Fig1_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 1\" aria-describedby=\"Fig1\" height=\"587\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"260 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular senescence in cancer: from mechanism paradoxes to precision therapeutics","authors":"Tiejun Feng, Fuda Xie, Leo M.Y. Lee, Zhiqiang Lin, Yifan Tu, Yang Lyu, Peiyao Yu, Jialin Wu, Bonan Chen, Ge Zhang, Gary M.K. Tse, Ka Fai To, Wei Kang","doi":"10.1186/s12943-025-02419-2","DOIUrl":"https://doi.org/10.1186/s12943-025-02419-2","url":null,"abstract":"Cellular senescence is a double-edged sword in cancer biology, functioning as both a tumor-suppressive mechanism and a driver of malignancy. Initially, senescence acts as a protective barrier by arresting the proliferation of damaged or oncogene-expressing cells via pathways such as oncogene-induced senescence and the DNA damage response. However, persistent senescence-associated secretory phenotype and metabolic reprogramming in senescent cells create a pro-inflammatory, immunosuppressive tumor microenvironment, fueling cancer progression, therapy resistance, and metastasis. This comprehensive review systematically examines the molecular mechanisms of senescence across diverse cancers, spanning digestive, reproductive, urinary, respiratory, nervous, hematologic, endocrine, and integumentary systems, and elucidates its context-dependent roles in tumor suppression and promotion. We highlight groundbreaking therapeutic innovations, including precision senolytics, senomorphics, and combinatorial strategies integrating immunotherapy, metabolic interventions, and epigenetic modulators. The review also addresses microenvironment remodeling and cutting-edge technologies for dissecting senescence heterogeneity, epigenetic clocks for biological age prediction, and microbiome engineering to modulate senescence. Despite their promise, challenges such as off-target effects, biomarker limitations, and cellular heterogeneity underscore the need for precision medicine approaches. Finally, we propose future directions to harness senescence as a dynamic therapeutic target, offering transformative potential for cancer treatment.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"35 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144797079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the glyco-immunity nexus in pancreatic cancer","authors":"Christabelle Rajesh, Richard D. Cummings, Prakash Radhakrishnan","doi":"10.1186/s12943-025-02417-4","DOIUrl":"https://doi.org/10.1186/s12943-025-02417-4","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive disease, and standard of care therapies have failed to yield significant clinical benefit, with invasive surgery being the only curative treatment for patients with early-stage disease. Tumor-associated glycans in pancreatic cancer have direct effects on the survival and propagation of the tumor proper and contribute to an immunosuppressed tumor microenvironment. The existence of a “tumor glycocode” in PDAC and the role of hypersialylation in this cancer have been hugely underscored. Through this initial understanding, significant strides have been made in the field of glycosylation-mediated immune regulation, uncovering glyco-immune checkpoints that facilitate tumor progression in PDAC and other malignancies. Here, we describe the specific roles of glycan-binding proteins, such as C-type lectin receptors, Siglecs, and Galectins, in generating and promoting immunosuppression, exacerbating survival outcomes, and dampening therapeutic efficacy. We illustrate the scale of glycan-mediated regulation of homeostatic immune responses and how cancer glycans facilitate dampened anti-tumor immunity through the major histocompatibility complex (MHC) and the enhanced expression of immune checkpoints, such as PD-L1 and CTLA-4. A wide array of glycan-targeted therapies against PDAC in the clinic, including monoclonal antibodies, enzymes, and vaccines, has been described. With the help of new glycosylation signatures identified and techniques that allow us to reach single-cell resolution, we can target glycans and generate strategies to activate the immune system against PDAC.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"58 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144769920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bispecific antibodies: unleashing a new era in oncology treatment","authors":"Lin Shui, Dan Wu, Kaixuan Yang, Chuntang Sun, Qingli Li, Rutie Yin","doi":"10.1186/s12943-025-02390-y","DOIUrl":"https://doi.org/10.1186/s12943-025-02390-y","url":null,"abstract":"Advancements in diagnostic and therapeutic standards have substantially enhanced the survival of patients with malignant tumors. Nevertheless, the quest for effective strategies to address resistant or recurrent advanced tumors remains a critical and unwavering objective. Bispecific antibodies (BsAbs) unleashed a new era of anti-tumor treatment by simultaneously binding to two distinct targets, thereby enhancing specificity, minimizing off-target toxicities, and synergistically modulating anti-tumor immunity and the tumor microenvironment. Compared with the combination of two monoclonal antibodies, BsAbs represent the physical integration of dual specificities, demonstrating superior binding efficacy, reducing the risk of drug resistance, and enabling unique biological functions such as bridging tumor cells and T cells to achieve precise cytotoxicity. However, limitations such as off-target toxicities, drug resistance and immune-related adverse effects require carefully evaluation and further optimization. Further studies are necessary to explore the potential of combining BsAbs with other anti-tumor strategies, balancing the efficacy and safety, optimizing the outpatient-based administration workflow. By tracking the research advancements of recently approved BsAbs and BsAb candidates in clinical trials, it is evident that BsAbs holds significant promise as a novel and transformative option for improving survival outcomes for patients. ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"13 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144769924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic checkpoints in immune cell reprogramming: rewiring immunometabolism for cancer therapy","authors":"Yingying Lv, Zongshang Li, Shutong Liu, Zhaokai Zhou, Jinling Song, Yuhao Ba, Siyuan Weng, Anning Zuo, Hui Xu, Peng Luo, Quan Cheng, Chuhan Zhang, Jingyuan Ning, Yukang Chen, Yuyuan Zhang, Zaoqu Liu, Xinwei Han","doi":"10.1186/s12943-025-02407-6","DOIUrl":"https://doi.org/10.1186/s12943-025-02407-6","url":null,"abstract":"Immune cell metabolism plays a pivotal role in regulating cellular proliferation, differentiation, and functional responses, collectively shaping immune responses within the tumor microenvironment (TME). Recent advancements increasingly highlight diverse metabolic phenotypes of immune cells and their complex interplay with tumor dynamics. Immune cell metabolism exhibits remarkable plasticity, enabling metabolic networks to finely tune immune cell behaviors in response to external stimuli. Furthermore, a strong correlation between metabolic profiles and immune cell fate, activation, and function has been repeatedly delineated in immunometabolism. Consequently, targeting the metabolic networks, referred to as metabolic checkpoints, to reprogram immune cell phenotypes and bolster antitumor immunity holds significant promise for clinical translation. This review summarizes the latest developments in multifaceted metabolic checkpoints, with a focus on how metabolic checkpoints modulate immunological consequences and cancer progression. Lastly, potential strategies for targeting metabolic checkpoints are explored to inspire innovative approaches in immunotherapy.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"724 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144763202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Traditional Chinese medicine in the treatment of breast Cancer","authors":"Peng Song, Tongtong Liu, Yinfang Zhang, Tingting Shao, Rongkun Li, Chaoxia An, Lu-Qi Cao, Zhe-Sheng Chen, Wenjing Guo, Dongzhu Duan","doi":"10.1186/s12943-025-02416-5","DOIUrl":"https://doi.org/10.1186/s12943-025-02416-5","url":null,"abstract":"Breast cancer (BC) is the most commonly diagnosed malignancy among women globally. While treatments such as chemotherapy and endocrine therapy have contributed to improving survival rates, there remains a critical need for more effective therapeutic options. Traditional Chinese Medicine (TCM), with a history spanning thousands of years, has long been utilized in the management of BC. This includes a wide range of practices, such as the use of traditional compound prescriptions, Chinese medicine monomers and extracts, acupuncture, moxibustion, and mind-body therapies. This review summarizes the brief history and experience of TCM in treating BC refer to numerous ancient Chinese medical texts, and explores the role of various TCM approaches in the treatment of BC, providing an in-depth analysis of their potential benefits. Additionally, it addresses the current limitations and challenges in researching TCM’s effectiveness for BC. Through this review, we aim to offer valuable insights into how TCM can complement conventional therapies and enhance outcomes for patients with BC.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"1 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144756360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}