Molecular Cancer最新文献

{"title":"Traditional Chinese medicine in lung cancer treatment","authors":"Zhichao Xi, Rongchen Dai, Yufei Ze, Xue Jiang, Mengfan Liu, Hongxi Xu","doi":"10.1186/s12943-025-02245-6","DOIUrl":"https://doi.org/10.1186/s12943-025-02245-6","url":null,"abstract":"Lung cancer remains a major global health challenge and one of the leading causes of cancer-related deaths worldwide. Despite significant advancements in treatment, challenges such as drug resistance, side effects, metastasis and recurrence continue to impact patient outcomes and quality of life. In response, there is growing interest in complementary and integrative approaches to cancer care. Traditional Chinese medicine (TCM), with its long history, abundant clinical experience, holistic perspective and individualized approach, has garnered increasing attention for its role in lung cancer prevention and management. This review provides a comprehensive overview of the advances in TCM for lung cancer treatment, covering its theoretical foundation, treatment principles, clinical experiences and evidence supporting its efficacy. We also provide a systematic summary of the preclinical mechanisms, through which TCM impacts lung cancer, including the induction of cell death, reversal of drug resistance, inhibition of metastasis and modulation of immune responses. Additionally, future prospects for TCM in lung cancer treatment are discussed, offering insights into its expanded application and integration with modern medicine to address this challenging disease.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"24 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143495364","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":"Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies","authors":"Ashkan Pouyan, Masoud Ghorbanlo, Masoud Eslami, Majid Jahanshahi, Ehsan Ziaei, Ali Salami, Khatere Mokhtari, Koorosh Shahpasand, Najma Farahani, Tohid Emami Meybodi, Maliheh Entezari, Afshin Taheriazam, Kiavash Hushmandi, Mehrdad Hashemi","doi":"10.1186/s12943-025-02267-0","DOIUrl":"https://doi.org/10.1186/s12943-025-02267-0","url":null,"abstract":"Glioblastoma multiforme (GBM) is the most prevalent and aggressive primary brain tumor in adults, characterized by a poor prognosis and significant resistance to existing treatments. Despite progress in therapeutic strategies, the median overall survival remains approximately 15 months. A hallmark of GBM is its intricate molecular profile, driven by disruptions in multiple signaling pathways, including PI3K/AKT/mTOR, Wnt, NF-κB, and TGF-β, critical to tumor growth, invasion, and treatment resistance. This review examines the epidemiology, molecular mechanisms, and therapeutic prospects of targeting these pathways in GBM, highlighting recent insights into pathway interactions and discovering new therapeutic targets to improve patient outcomes.\u0000","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"32 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143495363","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":"CircAKT3 promotes prostate cancer proliferation and metastasis by enhancing the binding of RPS27A and RPL11","authors":"Xiaoming Song, Ziwei Wei, Cong Zhang, Dunsheng Han, Jinke Liu, Yufeng Song, Xuefeng Xie, Dingchang Shao, Mingkun Zhao, Fan Chao, Guoxiong Xu, Shiyu Wang, Gang Chen","doi":"10.1186/s12943-025-02261-6","DOIUrl":"https://doi.org/10.1186/s12943-025-02261-6","url":null,"abstract":"Metastatic prostate cancer (PCa) is a leading cause of mortality among PCa patients. Although circular RNAs (circRNAs) are recognized for their pivotal roles in tumorigenesis, the specifics of their influence within the context of PCa have yet to be fully elucidated. RT-qPCR was conducted to evaluate circAKT3 expression in PCa cells and in both tumor and adjacent noncancerous tissues. The oncogenic role of circAKT3 was confirmed through a combination of in vitro and in vivo experiments. Mechanistic investigations using RNA-pulldown, RNA immunoprecipitation (RIP), fluorescence in situ hybridization (FISH), immunofluorescence (IF), and Chromatin Immunoprecipitation (ChIP) assays explored how circAKT3 modulates c-Myc activity via interactions with RPS27A and RPL11. Additionally, Western Blotting and further in vitro and in vivo studies assessed circAKT3's influence on PCa progression through MST1. This research identified the function and regulation of circAKT3, a circRNA derived from exons 2 to 8 of the kinase-b3 (AKT3) gene, in human PCa cells. CircAKT3 was significantly correlated with clinical indicators of disease severity, including D'Amico risk classification, the Gleason score, and pT stage. Both in vitro and in vivo experiments demonstrated that circAKT3 knockdown inhibited PCa cell proliferation, migration, and invasion. Lipid nanoparticles encapsulating si-circAKT3 (LNP-si-circAKT3) effectively suppressed the growth of bone tumors formed by PCa cells. Mechanistically, circAKT3 acted as a protein scaffold between ribosomal protein S27a (RPS27A) and ribosomal protein L11 (RPL11), promoting their cytoplasmic translocation and reducing nuclear RPL11 levels, ultimately diminishing RPL11’s interaction with c-Myc and resulting in enhanced c-Myc-driven suppression of macrophage stimulating 1 (MST1) expression. Consequently, the decreased MST1 led to PCa progression and metastasis. CircAKT3 formation was facilitated by both flanking Alu elements and the RNA binding protein Quaking (QKI). Additionally, downregulation of the RNA helicase URH49 resulted in the nuclear accumulation of circAKT3, finally suppressing MST1 expression. Our findings suggest that circAKT3 acts as a protein scaffold, promoting the interaction between RPS27A and RPL11, thereby influencing c-Myc activity and PCa progression. This study underscores the crucial role of circAKT3 in PCa and its potential as a therapeutic target to impede malignancy progression and metastasis.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"14 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143486358","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":"Role of circular RNAs in cancer therapy resistance","authors":"Wenjuan Liu, Jiling Niu, Yanfei Huo, Long Zhang, Linyu Han, Nasha Zhang, Ming Yang","doi":"10.1186/s12943-025-02254-5","DOIUrl":"https://doi.org/10.1186/s12943-025-02254-5","url":null,"abstract":"Over the past decade, circular RNAs (circRNAs) have gained recognition as a novel class of genetic molecules, many of which are implicated in cancer pathogenesis via different mechanisms, including drug resistance, immune escape, and radio-resistance. ExosomalcircRNAs, in particular, facilitatecommunication between tumour cells and micro-environmental cells, including immune cells, fibroblasts, and other components. Notably, micro-environmental cells can reportedly influence tumour progression and treatment resistance by releasing exosomalcircRNAs. circRNAs often exhibit tissue- and cancer-specific expression patterns, and growing evidence highlights their potential clinical relevance and utility. These molecules show strong promise as potential biomarkers and therapeutic targets for cancer diagnosis and treatment. Therefore, this review aimed to briefly discuss the latest findings on the roles and resistance mechanisms of key circRNAs in the treatment of various malignancies, including lung, breast, liver, colorectal, and gastric cancers, as well as haematological malignancies and neuroblastoma.This review will contribute to the identification of new circRNA biomarkers for the early diagnosis as well as therapeutic targets for the treatment of cancer.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"209 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143485779","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":"Cancer stem cells and niches: challenges in immunotherapy resistance","authors":"Yonglong Pan, Chaoyi Yuan, Chenglong Zeng, Chaoyang Sun, Limin Xia, Guihua Wang, Xiaoping Chen, Bixiang Zhang, Jianfeng Liu, Ze-yang Ding","doi":"10.1186/s12943-025-02265-2","DOIUrl":"https://doi.org/10.1186/s12943-025-02265-2","url":null,"abstract":"Cancer stem cells (CSCs) are central to tumor progression, metastasis, immune evasion, and therapeutic resistance. Characterized by remarkable self-renewal and adaptability, CSCs can transition dynamically between stem-like and differentiated states in response to external stimuli, a process termed “CSC plasticity.” This adaptability underpins their resilience to therapies, including immune checkpoint inhibitors and adoptive cell therapies (ACT). Beyond intrinsic properties, CSCs reside in a specialized microenvironment—the CSC niche—which provides immune-privileged protection, sustains their stemness, and fosters immune suppression. This review highlights the critical role of CSCs and their niche in driving immunotherapy resistance, emphasizing the need for integrative approaches to overcome these challenges.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"16 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143485781","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":"Spatial transcriptomic analysis of tumor microenvironment in esophageal squamous cell carcinoma with HIV infection","authors":"Yuanli Zuo, Yang Jin, Gang Li, Yue Ming, Ting Fan, Yitong Pan, Xiaojun Yao, Yong Peng","doi":"10.1186/s12943-025-02248-3","DOIUrl":"https://doi.org/10.1186/s12943-025-02248-3","url":null,"abstract":"Human Immunodeficiency Virus (HIV) is one of the most prevalent viruses, causing significant immune depletion in affected individuals. Current treatments can control HIV and prolong patients’ lives, but new challenges have emerged. Increasing incidence of cancers occur in HIV patients. Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers observed in HIV patients. However, the spatial cellular characteristics of HIV-related ESCC have not been explored, and the differences between HIV-ESCC and typical ESCC remain unclear. We performed spatial transcriptome sequencing on HIV-ESCC samples to depict the microenvironment and employed cell communication analysis and multiplex immunofluorescence to investigate the molecular mechanism in HIV-ESCC. We found that HIV-ESCC exhibited a unique cellular composition, with fibroblasts and epithelial cells intermixed throughout the tumor tissue, lacking obvious spatial separation, while other cell types were sparse. Besides, HIV-ESCC exhibited an immune desert phenotype, characterized by a low degree of immune cell infiltration, with only a few SPP1+ macrophages showing immune resistance functions. Cell communication analysis and multiplex immunofluorescence staining revealed that tumor fibroblasts in HIV-ESCC interact with CD44+ epithelial cells via COL1A2, promoting the expression of PIK3R1 in epithelial cells. This interaction activates the PI3K-AKT signaling pathway, which contributes to the progression of HIV-ESCC. Our findings depict the spatial microenvironment of HIV-ESCC and elucidate a molecular mechanism in the progression of HIV-ESCC. This will provide us insights into the molecular basis of HIV-ESCC and potential treatment strategies.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"14 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143485780","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":"Inflammation in cancer: therapeutic opportunities from new insights","authors":"Yifei Xie, Fangfang Liu, Yunfei Wu, Yuer Zhu, Yanan Jiang, Qiong Wu, Zigang Dong, Kangdong Liu","doi":"10.1186/s12943-025-02243-8","DOIUrl":"https://doi.org/10.1186/s12943-025-02243-8","url":null,"abstract":"As one part of the innate immune response to external stimuli, chronic inflammation increases the risk of various cancers, and tumor-promoting inflammation is considered one of the enabling characteristics of cancer development. Recently, there has been growing evidence on the role of anti-inflammation therapy in cancer prevention and treatment. And researchers have already achieved several noteworthy outcomes. In the review, we explored the underlying mechanisms by which inflammation affects the occurrence and development of cancer. The pro- or anti-tumor effects of these inflammatory factors such as interleukin, interferon, chemokine, inflammasome, and extracellular matrix are discussed. Since FDA-approved anti-inflammation drugs like aspirin show obvious anti-tumor effects, these drugs have unique advantages due to their relatively fewer side effects with long-term use compared to chemotherapy drugs. The characteristics make them promising candidates for cancer chemoprevention. Overall, this review discusses the role of these inflammatory molecules in carcinogenesis of cancer and new inflammation molecules-directed therapeutic opportunities, ranging from cytokine inhibitors/agonists, inflammasome inhibitors, some inhibitors that have already been or are expected to be applied in clinical practice, as well as recent discoveries of the anti-tumor effect of non-steroidal anti-inflammatory drugs and steroidal anti-inflammatory drugs. The advantages and disadvantages of their application in cancer chemoprevention are also discussed.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"8 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477502","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":"DCLK1-mediated regulation of invadopodia dynamics and matrix metalloproteinase trafficking drives invasive progression in head and neck squamous cell carcinoma","authors":"Levi Arnold, Marrion Yap, Nathan Farrokhian, Laura Jackson, Michael Barry, Thuc Ly, Pachiappan Arjunan, Angela Kaczorowski-Worthley, Carter Tews, Avisha Pandey, Austin Morrison, Michael P. Washburn, David Standing, Juan P. Gomez, Nanda Kumar Yellapu, David Johnson, Linheng Li, Shahid Umar, Shrikant Anant, Sufi Mary Thomas","doi":"10.1186/s12943-025-02264-3","DOIUrl":"https://doi.org/10.1186/s12943-025-02264-3","url":null,"abstract":"HNSCC presents a significant health challenge due to its high mortality resulting from treatment resistance and locoregional invasion into critical structures in the head and neck region. Understanding the invasion mechanisms of HNSCC has the potential to guide targeted therapies, improving patient survival. Previously, we demonstrated the involvement of doublecortin like kinase 1 (DCLK1) in regulating HNSCC cell invasion. Here, we investigated the hypothesis that DCLK1 modulates proteins within invadopodia, specialized subcellular protrusions that secrete matrix metalloproteinases to degrade the ECM. We employed tandem mass tag (TMT)-based proteomics to identify the role of DCLK1 in regulating proteins involved in HNSCC invasion and validated the findings using immunoblotting. The Cancer Genome Atlas (TCGA) database was interrogated to correlate DCLK1 expression with tumor stage, grade, and invasion-associated proteins. In vitro invasion was assessed using a Boyden chamber assay, and immunohistochemistry on patient samples determined DCLK1's distribution within tumors. Gelatin invadopodia assay was used to establish DCLK1 localization to invadopodia related gelatin degradation. Super-resolution confocal microscopy demonstrated colocalization of DCLK1 with invadopodia markers and MMP trafficking proteins. ECM degradation by MMPs in HNSCC cells with wild-type and knockdown DCLK1 was evaluated using a dye-quenched tracer, while gel zymography and MMP array identified secreted proteases. Proximity ligation assay (PLA) and co-immunoprecipitation assays were used to confirm interactions between DCLK1, MMP9, KIF16B, and RAB40B. Proteomic analysis demonstrate DCLK1's role in regulating proteins involved in cytoskeletal and ECM remodeling. Clinically, rising DCLK1 levels correlate with higher histological grade and lymph node metastasis, with heightened expression observed at the leading edge of HNSCC patient tissue. DCLK1 is localized with markers of mature invadopodia including TKS4, TKS5, cortactin, and MT1-MMP. Knockdown of DCLK1 led to reductions in invadopodia numbers and decreased in vitro invasion and ECM degradation. MMP9 colocalizes with DCLK1 within invadopodia structures and its secretion is disrupted by DCLK1 knockdown. Further, PLA and co-immunoprecipitations studies demonstrate DLCK1 complexes with KIF16B and RAB40B enabling trafficking of degradative MMP9 cargo along the invadopodia to degrade local ECM. This work unveils a novel function of DCLK1 in regulating KIF16B and RAB40B to traffic matrix degrading MMP9 cargo to the distal end of the invadopodia facilitating HNSCC invasion.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"31 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477707","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":"Single-cell RNA sequencing identifies molecular biomarkers predicting late progression to CDK4/6 inhibition in patients with HR+/HER2- metastatic breast cancer","authors":"Linjie Luo, Peng Yang, Sofia Mastoraki, Xiayu Rao, Yan Wang, Nicole M. Kettner, Akshara Singareeka Raghavendra, Debasish Tripathy, Senthil Damodaran, Kelly K. Hunt, Jing Wang, Ziyi Li, Khandan Keyomarsi","doi":"10.1186/s12943-025-02226-9","DOIUrl":"https://doi.org/10.1186/s12943-025-02226-9","url":null,"abstract":"Cyclin-dependent kinase 4/6 inhibitors (CDK4/6is) in combination with endocrine therapy are the standard treatment for patients with hormone receptor–positive, HER2–negative metastatic breast cancer (mBC). Despite the efficacy of CDK4/6is, intrinsic resistance occurs in approximately one-third of patients, highlighting the need for reliable predictive biomarkers. Single-cell RNA sequencing analyzed metastatic tumors from HR+/HER2- mBC patients pre-CDK4/6i treatment at baseline (BL) and/or at disease progression. BL samples were from CDK4/6i responders (median progression-free survival [mPFS] = 25.5 months), while progressors were categorized as early-progressors (EP, mPFS = 3 months) and late-progressors (LP, mPFS = 11 months). Metastatic sites included liver, pleural effusions, ascites, and bone. InferCNV distinguished tumor cells, and functional analysis utilized the Molecular Signatures Database. LP tumors displayed enhanced Myc, EMT, TNF-α, and inflammatory pathways compared to those EP tumors. Samples from BL and LP responders showed increased tumor-infiltrating CD8+ T cells and natural killer (NK) cells compared to EP non-responders. Notably, despite a high frequency of CD8+ T cells in responding tumors, a functional analysis revealed significant upregulation of genes associated with stress and apoptosis in proliferative CD4+ and CD8+ T cells in BL tumors compared to in EP and LP tumors. These genes, including HSP90 and HSPA8, are linked to resistance to PD1/PD-L1 immune checkpoint inhibitors. A ligand-receptor analysis showed enhanced interactions associated with inhibitory T-cell proliferation (SPP1-CD44) and suppression of immune activity (MDK-NCL) in LP tumors. Longitudinal biopsies consistently revealed dynamic NK cell expansion and enhanced cytotoxic T cell activity, alongside upregulation of immune activity inhibition, in LP tumors compared to in BL tumors. Notably, the predictive biomarker panel from BL tumor cells was validated in 2 independent cohorts, where it consistently predicted a significant improvement in mPFS duration in signature-high versus -low groups. This study underscores the significance of molecular biomarkers in predicting clinical outcomes to CDK4/6i. Tumor-infiltration CD8+ T and NK cells may also serve as baseline predictors. These insights pave the way for optimizing therapeutic strategies based on microenvironment-specific changes, providing a personalized and effective approach for managing HR+/HER2- mBC and improving patient outcomes.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"79 6 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143417305","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":"Correction: Deciphering a profiling based on multiple post-translational modifications functionally associated regulatory patterns and therapeutic opportunities in human hepatocellular carcinoma","authors":"Yuanxiang Lao, Yirong Jin, Songfeng Wu, Ting Fang, Qiang Wang, Longqin Sun, Beicheng Sun","doi":"10.1186/s12943-025-02268-z","DOIUrl":"https://doi.org/10.1186/s12943-025-02268-z","url":null,"abstract":"<p><b>Correction: </b><b><i>Mol Cancer </i></b><b>23, 283 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02199-1</b></p><p>Following the publication of the original article [1], the author has requested the publication of an erratum to address the following issues stated below.</p><ul>\u0000<li>\u0000<p>An article note that says, “Yuanxiang Lao, Yirong Jin, and Songfeng Wu are co-first authors. \" should be added to the manuscript.</p>\u0000</li>\u0000<li>\u0000<p>The Supplementary Material 1 should be replaced with the one provided in the Supplementary Informtion in this correction article.</p>\u0000</li>\u0000<li>\u0000<p>The second “Extended data Fig. 3c” should be “Extended data Fig. 3d”, and “Extended Data Fig. 3d” as well as “Extended Data Fig. 3e-f” should be “Extended Data Fig. 3e” and “Extended Data Fig. 3f”, respectively.</p>\u0000</li>\u0000<li>\u0000<p>The figure citation “Extended Data Fig. 5g” should be “Extended Data Fig. 5f”.</p>\u0000</li>\u0000<li>\u0000<p>The figure citation “Extended Data Fig. 8d-e” should be “Extended Data Fig. 8d-g”.</p>\u0000</li>\u0000</ul><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Lao Y, Jin Y, Wu S, et al. Deciphering a profiling based on multiple post-translational modifications functionally associated regulatory patterns and therapeutic opportunities in human hepatocellular carcinoma. Mol Cancer. 2024;23:283. https://doi.org/10.1186/s12943-024-02199-1.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><span>Author notes</span><ol><li><p>Yuanxiang Lao, Yirong Jin, and Songfeng Wu are co-first authors.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>Department of Hepatobiliary Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China</p><p>Yuanxiang Lao, Yirong Jin, Ting Fang, Qiang Wang & Beicheng Sun</p></li><li><p>Anhui Province Key Laboratory of Tumor Immune Microenvironment and Immunotherapy, Innovative Institute of Tumor Immunity and Medicine (ITIM), Hefei, Anhui, China</p><p>Yuanxiang Lao, Yirong Jin, Ting Fang, Qiang Wang & Beicheng Sun</p></li><li><p>Anhui Provincial Innovation Institute for Pharmaceutical Basic Research, Hefei, Anhui, China</p><p>Yuanxiang Lao, Yirong Jin, Ting Fang, Qiang Wang & Beicheng Sun</p></li><li><p>Beijing Qinglian Biotech Co., Ltd, Beijing, China</p><p>Songfeng Wu & Longqin Sun</p></li></ol><span>Authors</span><ol><li><span>Yuanxiang Lao</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yirong Jin</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Songfeng Wu</span>View author publications<p>You can also search for this author in","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"47 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143417306","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}