Molecular Cancer最新文献

{"title":"Extracellular vesicles in tumor immunity: mechanisms and novel insights","authors":"Liwen Kuang, Lei Wu, Yongsheng Li","doi":"10.1186/s12943-025-02233-w","DOIUrl":"https://doi.org/10.1186/s12943-025-02233-w","url":null,"abstract":"Extracellular vesicles (EVs), nanoscale vesicles secreted by cells, have attracted considerable attention in recent years due to their role in tumor immunomodulation. These vesicles facilitate intercellular communication by transporting proteins, nucleic acids, and other biologically active substances, and they exhibit a dual role in tumor development and immune evasion mechanisms. Specifically, EVs can assist tumor cells in evading immune surveillance and attack by impairing immune cell function or modulating immunosuppressive pathways, thereby promoting tumor progression and metastasis. Conversely, they can also transport and release immunomodulatory factors that stimulate the activation and regulation of the immune system, enhancing the body’s capacity to combat malignant diseases. This dual functionality of EVs presents promising avenues and targets for tumor immunotherapy. By examining the biological characteristics of EVs and their influence on tumor immunity, novel therapeutic strategies can be developed to improve the efficacy and relevance of cancer treatment. This review delineates the complex role of EVs in tumor immunomodulation and explores their potential implications for cancer therapeutic approaches, aiming to establish a theoretical foundation and provide practical insights for the advancement of future EVs-based cancer immunotherapy strategies.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"64 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143418413","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":"Hijacking of the nervous system in cancer: mechanism and therapeutic targets","authors":"Yu Zhang, Qili Liao, Xuyang Wen, Jiayan Fan, Tifei Yuan, Xuemei Tong, Renbing Jia, Peiwei Chai, Xianqun Fan","doi":"10.1186/s12943-025-02246-5","DOIUrl":"https://doi.org/10.1186/s12943-025-02246-5","url":null,"abstract":"The activity of neurons in the vicinity of tumors is linked to a spectrum of cellular mechanisms, including the facilitation of tumor cell proliferation, synapse formation, angiogenesis, and macrophage polarization. This review consolidates the current understanding of neuro-oncological regulation, underscoring the nuanced interplay between neurological and oncological processes (termed as Cancer-Neuroscience). First, we elucidated how the nervous system accelerates tumor growth, metastasis, and the tumor microenvironment both directly and indirectly through the action of signaling molecules. Importantly, neural activity is also implicated in modulating the efficacy of therapeutic interventions, including immunotherapy. On the contrary, the nervous system potentially has a suppressive effect on tumorigenesis, further underscoring a dual-edged role of neurons in cancer progression. Consequently, targeting specific signaling molecules within neuro-oncological regulatory pathways could potentially suppress tumor development. Future research is poised to explore the intricate mechanisms governing neuro-tumor interactions more deeply, while concurrently refining treatment strategies for tumors by targeting the crosstalk between cancer and neurons.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"22 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143191924","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":"Multimodal lung cancer theranostics via manganese phosphate/quercetin particle","authors":"Chong Qiu, Fei Xia, Qingchao Tu, Huan Tang, Yinan Liu, Hongda Liu, Chen Wang, HaiLu Yao, Linying Zhong, Yuanfeng Fu, Pengbo Guo, Weiqi Chen, Xinyu Zhou, Li Zou, Licheng Gan, Jiawei Yan, Yichong Hou, Junzhe Zhang, Huanhuan Pang, Yuqing Meng, Qiaoli Shi, Guang Han, Xijun Wang, Jigang Wang","doi":"10.1186/s12943-025-02242-9","DOIUrl":"https://doi.org/10.1186/s12943-025-02242-9","url":null,"abstract":"The diagnosis and treatment of non-small cell lung cancer in clinical settings face serious challenges, particularly due to the lack of integration between the two processes, which limit real-time adjustments in treatment plans based on the patient’s condition and drive-up treatment costs. Here, we present a multifunctional pH-sensitive core-shell nanoparticle containing quercetin (QCT), termed AHA@MnP/QCT NPs, designed for the simultaneous diagnosis and treatment of non-small cell lung cancer. Mechanistic studies indicated that QCT and Mn2+ exhibited excellent peroxidase-like (POD-like) activity, catalysing the conversion of endogenous hydrogen peroxide into highly toxic hydroxyl radicals through a Fenton-like reaction, depleting glutathione (GSH), promoting reactive oxygen species (ROS) generation in mitochondria and endoplasmic reticulum, and inducing ferroptosis. Additionally, Mn2+ could activate the cGAS-STING signalling pathway and promote the maturation of dendritic cells and infiltration of activated T cells, thus inducing tumor immunogenic cell death (ICD). Furthermore, it exhibited effective T2-weighted MRI enhancement for tumor imaging, making them valuable for clinical diagnosis. In vitro and in vivo experiments demonstrated that AHA@MnP/QCT NPs enabled non-invasive imaging and tumor treatment, which presented a one-stone-for-two-birds strategy for combining tumor diagnosis and treatment, with broad potential for clinical application in non-small cell lung cancer therapy. ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"22 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143083322","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: The landscape of BRAF transcript and protein variants in human cancer","authors":"Andrea Marranci, Zhijie Jiang, Marianna Vitiello, Elena Guzzolino, Laura Comelli, Samanta Sarti, Simone Lubrano, Cinzia Franchin, Ileabett Echevarría-Vargas, Andrea Tuccoli, Alberto Mercatanti, Monica Evangelista, Paolo Sportoletti, Giorgio Cozza, Ettore Luzi, Enrico Capobianco, Jessie Villanueva, Giorgio Arrigoni, Giovanni Signore, Silvia Rocchiccioli, Letizia Pitto, Nicholas Tsinoremas, Laura Poliseno","doi":"10.1186/s12943-025-02241-w","DOIUrl":"https://doi.org/10.1186/s12943-025-02241-w","url":null,"abstract":"<p><b>Correction</b><b>: </b><b>Mol Cancer 16, 85 (2017)</b></p><p><b>https://doi.org/10.1186/s12943-017-0645-4</b></p><br/><p>Following the publication of the original article [1], the authors would like to update Figure 8. They noticed that the graph in panel d was erroneously duplicated in panel h during the production process. The incorrect and correct figures are provided below.</p><p>Incorrect Figure 8:</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02241-w/MediaObjects/12943_2025_2241_Figa_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure a\" aria-describedby=\"Figa\" height=\"942\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02241-w/MediaObjects/12943_2025_2241_Figa_HTML.png\" width=\"685\"/></picture></figure><p>Correct Figure 8:</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02241-w/MediaObjects/12943_2025_2241_Figb_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure b\" aria-describedby=\"Figb\" height=\"928\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02241-w/MediaObjects/12943_2025_2241_Figb_HTML.png\" width=\"685\"/></picture></figure><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Marranci A, Jiang Z, Vitiello M, et al. The landscape of <i>BRAF</i> transcript and protein variants in human cancer. Mol Cancer. 2017;16:85. https://doi.org/10.1186/s12943-017-0645-4.</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>Equal contributors</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>Oncogenomics Unit, Core Research Laboratory, Istituto Toscano Tumori (ITT), AOUP, CNR-IFC, Via Moruzzi 1, 56124, Pisa, Italy</p><p>Andrea Marranci, Marianna Vitiello, Samanta Sarti, Simone Lubrano, Andrea Tuccoli & Laura Poliseno</p></li><li><p>University of Siena, Siena, Italy</p><p>Andrea Marranci, Samanta Sarti & Simone Lubrano</p></li><li><p>Center for Computational Science, University of Miami, Gables One Tower, Room 600 N, 1320 S. Dixie Highway, Coral Gables, FL, 33146-2926, USA</p><p>Zhijie Jiang, Enrico Capobianco & Nicholas Tsinoremas</p></li><li><p>Scuola Superiore Sant’Anna, Pisa, Italy</p><p>Elena Guzzolino</p></li><li><p>Institute of Clinical Physiology (IFC), CNR, Via Moruzzi 1, 56124, Pisa, Italy</p><p>Marianna Vitiello, Laura Comelli, Alberto Mercatanti, Monica Evangelista, Silvia Rocchiccioli, Letizia Pitto & Laura Poliseno</p></li><li><p>Department of Biomedical Sciences, University of Padova, Padua, Italy</p><p>Cinzia Franchin & Giorgio Arrigoni</p></li","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"8 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143077465","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 cells avoid ferroptosis induced by immune cells via fatty acid binding proteins","authors":"Maria Angelica Freitas-Cortez, Fatemeh Masrorpour, Hong Jiang, Iqbal Mahmud, Yue Lu, Ailing Huang, Lisa K. Duong, Qi Wang, Tiffany A. Voss, Claudia S. Kettlun Leyton, Bo Wei, Wai-Kin Chan, Kevin Lin, Jie Zhang, Efrosini Tsouko, Shonik Ganjoo, Hampartsoum B. Barsoumian, Thomas S. Riad, Yun Hu, Carola Leuschner, Nahum Puebla-Osorio, Jing Wang, Jian Hu, Michael A. Davies, Vinay K. Puduvalli, Cyrielle Billon, Thomas P. Burris, Philip L. Lorenzi, Boyi Gan, James W. Welsh","doi":"10.1186/s12943-024-02198-2","DOIUrl":"https://doi.org/10.1186/s12943-024-02198-2","url":null,"abstract":"Cancer creates an immunosuppressive environment that hampers immune responses, allowing tumors to grow and resist therapy. One way the immune system fights back is by inducing ferroptosis, a type of cell death, in tumor cells through CD8 + T cells. This involves lipid peroxidation and enzymes like lysophosphatidylcholine acyltransferase 3 (Lpcat3), which makes cells more prone to ferroptosis. However, the mechanisms by which cancer cells avoid immunotherapy-mediated ferroptosis are unclear. Our study reveals how cancer cells evade ferroptosis and anti-tumor immunity through the upregulation of fatty acid-binding protein 7 (Fabp7). To explore how cancer cells resist immune cell-mediated ferroptosis, we used a comprehensive range of techniques. We worked with cell lines including PD1-sensitive, PD1-resistant, B16F10, and QPP7 glioblastoma cells, and conducted in vivo studies in syngeneic 129 Sv/Ev, C57BL/6, and conditional knockout mice with Rora deletion specifically in CD8+ T cells, Cd8 cre;Rorafl mice. Methods included mass spectrometry-based lipidomics, targeted lipidomics, Oil Red O staining, Seahorse analysis, quantitative PCR, immunohistochemistry, PPARγ transcription factor assays, ChIP-seq, untargeted lipidomic analysis, ROS assay, ex vivo co-culture of CD8+ T cells with cancer cells, ATAC-seq, RNA-seq, Western blotting, co-immunoprecipitation assay, flow cytometry and Imaging Mass Cytometry. PD1-resistant tumors upregulate Fabp7, driving protective metabolic changes that shield cells from ferroptosis and evade anti-tumor immunity. Fabp7 decreases the transcription of ferroptosis-inducing genes like Lpcat3 and increases the transcription of ferroptosis-protective genes such as Bmal1 through epigenetic reprogramming. Lipidomic profiling revealed that Fabp7 increases triglycerides and monounsaturated fatty acids (MUFAs), which impede lipid peroxidation and ROS generation. Fabp7 also improves mitochondrial function and fatty acid oxidation (FAO), enhancing cancer cell survival. Furthermore, cancer cells increase Fabp7 expression in CD8+ T cells, disrupting circadian clock gene expression and triggering apoptosis through p53 stabilization. Clinical trial data revealed that higher FABP7 expression correlates with poorer overall survival and progression-free survival in patients undergoing immunotherapy. Our study uncovers a novel mechanism by which cancer cells evade immune-mediated ferroptosis through Fabp7 upregulation. This protein reprograms lipid metabolism and disrupts circadian regulation in immune cells, promoting tumor survival and resistance to immunotherapy. Targeting Fabp7 could enhance immunotherapy effectiveness by re-sensitizing resistant tumors to ferroptosis.\u0000","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"11 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143077464","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":"SELP+ TEC:CD8+ T cell crosstalk associates with improved radiotherapy efficacy in cervical cancer","authors":"Qingyu Huang, Wenhui Yang, Fuhao Wang, Rui Huang, Qian Wang, Xiaohui Li, Tianyu Lei, Shengqin Yue, Wenxue Zou, Qi An, Jinbo Yue, Qinyong Hu, Chao Liu","doi":"10.1186/s12943-025-02244-7","DOIUrl":"https://doi.org/10.1186/s12943-025-02244-7","url":null,"abstract":"P-selectin (SELP) expression in tumor cells has been implicated in promoting tumor progression and treatment resistance across various cancers. However, our prior study identified SELP expression in a specific subpopulation of endothelial cells within cervical cancer (CC) and potentially linked to anti-cancer immune response. The precise mechanisms by which SELP influences anti-cancer immunity and its involvement in radiotherapy response in CC, however, remain elusive. To address these gaps, this study analyzed tumor tissue samples from 205 CC patients undergoing radiotherapy, scRNA-seq data from 42,159 cells of eight patients, and bulk RNA-sequencing data from 187 radiotherapy-treated patients. The results revealed that elevated SELP expression in tumor endothelial cells (TECs) was significantly correlated with improved survival outcomes in patients treated with radiotherapy. The SELPhigh group exhibited a prominent enrichment of immune-related pathways, coupled with a diminished enrichment in epithelial cell proliferation and angiogenesis pathways. Notably, this group demonstrated increased infiltration of CD8+ T cells and enhanced expression of chemokine receptors, including ACKR1. Furthermore, our data suggest that SELP+ TECs engage in crosstalk with CD8+ T cells via the ACKR1-CCL5 axis, which is associated with improved radiotherapy efficacy. In conclusion, these findings underscore the pivotal role of SELP+ TEC:CD8+ T cell interactions through the ACKR1-CCL5 pathway in enhancing radiotherapy response in CC. Targeting this crosstalk may offer novel therapeutic strategies to mitigate treatment resistance and improve patient survival.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"28 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143077462","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":"CircRNF13 enhances IGF2BP1 phase separation-mediated ITGB1 mRNA stabilization in an m6A-dependent manner to promote oral cancer cisplatin chemoresistance","authors":"Xuemeng Xu, Qiu Peng, Zongyao Ren, Yaqian Han, Xianjie Jiang, Zhu Wu, Shiming Tan, Wenjuan Yang, Linda Oyang, Xia Luo, Jinguan Lin, Longzheng Xia, Mingjing Peng, Nayiyuan Wu, Yanyan Tang, Hao Tian, Yujuan Zhou, Qianjin Liao","doi":"10.1186/s12943-025-02239-4","DOIUrl":"https://doi.org/10.1186/s12943-025-02239-4","url":null,"abstract":"Oral cancer ranks among the most common malignancies within the head and neck region; however, its etiology remains inadequately understood despite substantial research advances in recent years. Many studies highlight the regulatory role of circular RNAs (circRNAs) in human cancers, suggesting their potential as cancer biomarkers. However, their specific mechanisms in oral cancer are not well understood. This study analyzed circRNAs expression in oral cancer, identifying circRNF13 (circbaseID: has_circ_0006801) as having elevated expression in oral cancer cells and tissues. Our study demonstrated that circRNF13 is correlated with increased tumor grade and stage in oral cancer. Results from both in vitro and in vivo experiments indicated that circRNF13 enhances cancer cell proliferation and tumor growth, while concurrently diminishing tumor sensitivity to cisplatin. Mechanistically, circRNF13 interacts with the m6A “reader” protein IGF2BP1, inhibiting its ubiquitin-mediated degradation and promoting its phase separation formation. Subsequently, circRNF13 augments the stability of ITGB1 mRNA via IGF2BP1 in a manner dependent on m6A modification. The m6A modification of ITGB1 mRNA is modulated by the phase separation of IGF2BP1, thereby promoting the malignant progression of oral cancer cells. This evidence positions circRNF13 as a crucial regulatory molecule in the pathogenesis of oral cancer and suggests its potential as a therapeutic target. This discovery enriches our understanding of the mechanistic role of circRNAs.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"128 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143072130","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: YTHDF2 in peritumoral hepatocytes mediates chemotherapy-induced antitumor immune responses through CX3CL1-mediated CD8+ T cell recruitment","authors":"Zhenyun Yang, Xin Wang, Yizhen Fu, Weijie Wu, Zili Hu, Qingyang Lin, Wei Peng, Yangxun Pan, Juncheng Wang, Jinbin Chen, Dandan Hu, Zhongguo Zhou, Li Xu, Yaojun Zhang, Jiajie Hou, Minshan Chen","doi":"10.1186/s12943-025-02252-7","DOIUrl":"https://doi.org/10.1186/s12943-025-02252-7","url":null,"abstract":"<p><b>Correction</b>: <b><i>Mol Cancer</i></b><b> 23</b>,<b> 186 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02097-6</b></p><p>Following publication of the original article [1], it was noted that the authors inadvertently left out the major funding source in the Funding information section, which was highly dependent throughout the study. Therefore, they requested to update the information under the Funding section. The original article has been corrected.</p><p> The Funding information currently reads:</p><p>\u0000<b>Fundings</b></p><p>This work is funded by the National Natural Science Foundation of China (No: 81874070 to M.S. Chen, 82073243 to X. Wang, 82103566 to D.D. Hu ), Guangdong Basic and Applied Basic Research Foundation (2022A1515110961 to J.C. Wang), Guangzhou Science and Technology Plan Project (2023A04J2125 to J.C. Wang), the China Postdoctoral Science Foundation (No: 2023M744018 to Y.Z. Fu).</p><p> The Funding information should read:</p><p>\u0000<b>Fundings</b></p><p>This work is funded by the Guangdong Provincial Science Fund for Distinguished Young Scholars (2021B1515020007, to J.Hou), the National Natural Science Foundation of China (No: 81874070 to M.S. Chen, 82073243 to X. Wang, 82103566 to D.D. Hu), Guangdong Basic and Applied Basic Research Foundation (2022A1515110961 to J.C. Wang), Guangzhou Science and Technology Plan Project (2023A04J2125 to J.C. Wang), the China Postdoctoral Science Foundation (No: 2023M744018 to Y.Z. Fu).</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Yang Z, Wang X, Fu Y, et al. YTHDF2 in peritumoral hepatocytes mediates chemotherapy-induced antitumor immune responses through CX3CL1-mediated CD8<sup>+</sup> T cell recruitment. Mol Cancer. 2024;23:186. https://doi.org/10.1186/s12943-024-02097-6.</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><h3>Authors and Affiliations</h3><ol><li><p>Department of Liver Surgery, Sun Yat-sen University Cancer Center, Guangzhou, 510060, Guangdong, People’s Republic of China</p><p>Zhenyun Yang, Xin Wang, Yizhen Fu, Weijie Wu, Zili Hu, Qingyang Lin, Wei Peng, Yangxun Pan, Juncheng Wang, Jinbin Chen, Dandan Hu, Zhongguo Zhou, Li Xu, Yaojun Zhang & Minshan Chen</p></li><li><p>Collaborative Innovation Center for Cancer Medicine, State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, Guangdong, People’s Republic of China</p><p>Zhenyun Yang, Xin Wang, Yizhen Fu, Weijie Wu, Zili Hu, Qingyang Lin, Wei Peng, Yangxun Pan, Juncheng Wang, Jinbin Chen, Dandan Hu, Zhongguo Zhou, Li Xu, Yaojun Zhang & Minshan Chen</p></li><li><p>State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Collab","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"41 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143071852","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":"lncRNAs: the unexpected link between protein synthesis and cancer adaptation","authors":"Mila Gugnoni, Manoj Kumar Kashyap, Kishore K. Wary, Alessia Ciarrocchi","doi":"10.1186/s12943-025-02236-7","DOIUrl":"https://doi.org/10.1186/s12943-025-02236-7","url":null,"abstract":"Cancer progression relies on the ability of cells to adapt to challenging environments overcoming stresses and growth constraints. Such adaptation is a multifactorial process that depends on the rapid reorganization of many basic cellular mechanisms. Protein synthesis is often dysregulated in cancer, and translational reprogramming is emerging as a driving force of cancer adaptive plasticity. Long non-coding RNAs (lncRNAs) represent the main product of genome transcription. They outnumber mRNAs by an order of magnitude and their expression is regulated in an extremely specific manner depending on context, space and time. This heterogeneity is functional and allows lncRNAs to act as context-specific, fine-tuning controllers of gene expression. Multiple recent evidence underlines how, besides their consolidated role in transcription, lncRNAs are major players in translation control. Their capacity to establish multiple and highly dynamic interactions with proteins and other transcripts makes these molecules able to play a central role across all phases of protein synthesis. Even if through a myriad of different mechanisms, the action of these transcripts is dual. On one hand, by modulating the overall translation speed, lncRNAs participate in the process of metabolic adaptation of cancer cells under stress conditions. On the other hand, by prioritizing the synthesis of specific transcripts they help cancer cells to maintain high levels of essential oncogenes. In this review, we aim to discuss the most relevant evidence regarding the involvement of lncRNAs in translation regulation and to discuss how this specific function may affect cancer plasticity and resistance to stress. We also expect to provide one of the first collective perspectives on the way these transcripts modulate gene expression beyond transcription.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"27 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143071858","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: miR-630 targets IGF1R to regulate response to HER-targeting drugs and overall cancer cell progression in HER2 over-expressing breast cancer","authors":"Claire Corcoran, Sweta Rani, Susan Breslin, Martina Gogarty, Irene M Ghobrial, John Crown, Lorraine O’Driscoll","doi":"10.1186/s12943-025-02251-8","DOIUrl":"https://doi.org/10.1186/s12943-025-02251-8","url":null,"abstract":"<p><b>Correction</b><b>: </b><b>Mol Cancer 13, 71 (2014)</b></p><p><b>https://doi.org/10.1186/1476-4598-13-71</b></p><br/><p>Following the publication of the original article [1], the authors would like to update Figure 4 as the SKBR3-LR NC mimic migration image presented in the published article was incorrect, but the associated graph showing % fold change was correct. The error was due to a pasting error when compiling the composite figure (two NC mimic invasion images were inadvertently pasted, instead of one NC mimic migration and one NC mimic invasion image). The incorrect and correct figures are provided below.</p><p>Incorrect Figure 4:</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figa_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure a\" aria-describedby=\"Figa\" height=\"535\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figa_HTML.png\" width=\"685\"/></picture></figure><p>Correct Figure 4:</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figb_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure b\" aria-describedby=\"Figb\" height=\"532\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figb_HTML.png\" width=\"685\"/></picture></figure><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Corcoran C, Rani S, Breslin S, et al. miR-630 targets IGF1R to regulate response to HER-targeting drugs and overall cancer cell progression in HER2 over-expressing breast cancer. Mol Cancer. 2014;13:71. https://doi.org/10.1186/1476-4598-13-71.</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><h3>Authors and Affiliations</h3><ol><li><p>School of Pharmacy and Pharmaceutical Sciences & Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland</p><p>Claire Corcoran, Sweta Rani, Susan Breslin, Martina Gogarty & Lorraine O’Driscoll</p></li><li><p>Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA</p><p>Irene M Ghobrial</p></li><li><p>Department of Oncology, St. Vincent’s University Hospital, Dublin 4, Ireland</p><p>John Crown</p></li></ol><span>Authors</span><ol><li><span>Claire Corcoran</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Sweta Rani</span>View author publications<p>You can also search for this author in <span>PubMed<span>","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"24 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143072128","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}