Molecular Cancer最新文献

{"title":"The application of organoids in investigating immune evasion in the microenvironment of gastric cancer and screening novel drug candidates","authors":"Liuyue Kan, Ying Yu, Yaxue Wang, Lei Shi, Tingyuan Fan, Hui Chen, Chuanli Ren","doi":"10.1186/s12943-025-02328-4","DOIUrl":"https://doi.org/10.1186/s12943-025-02328-4","url":null,"abstract":"Gastric cancer (GC) is a prevalent digestive system tumor, the fifth most diagnosed cancer worldwide, and a leading cause of cancer deaths. GC is distinguished by its pronounced heterogeneity and a dynamically evolving tumor microenvironment (TME). The lack of accurate disease models complicates the understanding of its mechanisms and impedes the discovery of novel drugs. A growing body of evidence suggests that GC organoids, developed using organoid culture technology, preserve the genetic, phenotypic, and behavioral characteristics. GC organoids hold significant potential for predicting treatment responses in individual patients. This review provides a comprehensive overview of the current clinical treatment strategies for GC, as well as the history, construction and clinical applications of organoids. The focus is on the role of organoids in simulating the TME to explore mechanisms of immune evasion and intratumoral microbiota in GC, as well as their applications in guiding clinical drug therapy and facilitating novel drug screening. Furthermore, we summarize the limitations of GC organoid models and underscore the need for continued technological advancements to benefit both basic and translational oncological research.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"44 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143875887","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":"Advancing pancreatic cancer therapy by mesothelin-specific nanobody conjugation","authors":"Soyeon Yi, Kyunghee Noh, Hyeran Kim, Eunkyeong Jung, Suhyeon Kim, Jieun Lee, Kyeonghye Guk, Jinsol Choi, Eun-Kyung Lim, Seokho Kim, Hwangseo Park, Jung Hwa Lim, Cho-Rok Jung, Taejoon Kang, Juyeon Jung","doi":"10.1186/s12943-025-02325-7","DOIUrl":"https://doi.org/10.1186/s12943-025-02325-7","url":null,"abstract":"Pancreatic adenocarcinoma (PAAD) is highly challenging to treat due to its poor prognosis and limited effective treatment options. Liposomal nanotechnology has emerged as a promising drug delivery platform in oncology, but existing liposomal therapies face limitations such as systemic toxicity, insufficient tumor selectivity, and low target specificity. Mesothelin (MSLN), an antigen overexpressed in PAAD, has attracted attention as a potential target for precision therapy. Here, we present the development of an anti-MSLN nanobody (D3 Nb) with high binding affinity (KD = 2.2 nM) that can selectively bind to MSLN-positive cancer cells. Structural analysis revealed that hydrophobic and hydrogen bonds within the complementary determining region (CDR) of D3 Nb promote strong binding to MSLN, leading to significant inhibition of AKT/NF-κB signaling and downregulation of fibronectin 1 (FN1) and twist1, key drivers of PAAD oncogenicity. In vivo studies confirmed that D3 Nb alone inhibits tumor progression. Furthermore, selective delivery to MSLN-positive tumors in combination with gemcitabine-loaded liposomes (D3-LNP-GEM) significantly improved cytotoxicity and promoted tumor regression. These findings highlight the potential of the D3-LNP-GEM platform as a novel targeted therapy for MSLN-expressing malignancies, showing promising efficacy in preclinical models and paving the way for continued clinical evaluation.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"2 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866834","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":"LSD1 inhibition attenuates targeted therapy-induced lineage plasticity in BRAF mutant colorectal cancer","authors":"Christopher A. Ladaika, Averi Chakraborty, Ashiq Masood, Galen Hostetter, Joo Mi Yi, Heather M. O’Hagan","doi":"10.1186/s12943-025-02311-z","DOIUrl":"https://doi.org/10.1186/s12943-025-02311-z","url":null,"abstract":"BRAF activating mutations occur in approximately 10% of metastatic colorectal cancer (CRCs) and are associated with worse prognosis in part due to an inferior response to standard chemotherapy. Standard of care for patients with refractory metastatic BRAFV600E CRC is treatment with BRAF and EGFR inhibitors and recent FDA approval was given to use these inhibitors in combination with chemotherapy for patients with treatment naïve metastatic BRAFV600E CRC. Lineage plasticity to neuroendocrine cancer is an emerging mechanism of targeted therapy resistance in several cancer types. Enteroendocrine cells (EECs), the neuroendocrine cell of the intestine, are uniquely present in BRAF mutant CRC as compared to BRAF wildtype CRC. BRAF plus EGFR inhibitor treatment induced changes in cell composition were determined by gene expression, imaging and single cell approaches in multiple models of BRAF mutant CRC. Furthermore, multiple clinically relevant inhibitors of the lysine demethylase LSD1 were tested to determine which inhibitor blocked the changes in cell composition. Combined BRAF and EGFR inhibition enriched for EECs in all BRAF mutant CRC models tested. Additionally, EECs and other secretory cell types were enriched in a subset of BRAFV600E CRC patient samples following targeted therapy. Importantly, inhibition of LSD1 with a clinically relevant inhibitor attenuated targeted therapy-induced EEC enrichment through blocking the interaction of LSD1, CoREST2 and STAT3. Our findings that BRAF plus EGFR inhibition induces lineage plasticity in BRAFV600E CRC represents a new paradigm for how resistance to BRAF plus EGFR inhibition occurs. Additionally, our finding that LSD1 inhibition blocks lineage plasticity has the potential to improve responses to BRAF plus EGFR inhibitor therapy in patients.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"24 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143862709","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":"Emerging artificial intelligence-driven precision therapies in tumor drug resistance: recent advances, opportunities, and challenges","authors":"Yuan Mao, Dangang Shangguan, Qi Huang, Ling Xiao, Dongsheng Cao, Hui Zhou, Yi-Kun Wang","doi":"10.1186/s12943-025-02321-x","DOIUrl":"https://doi.org/10.1186/s12943-025-02321-x","url":null,"abstract":"Drug resistance is one of the main reasons for cancer treatment failure, leading to a rapid recurrence/disease progression of the cancer. Recently, artificial intelligence (AI) has empowered physicians to use its powerful data processing and pattern recognition capabilities to extract and mine valuable drug resistance information from large amounts of clinical or omics data, to study drug resistance mechanisms, to evaluate and predict drug resistance, and to develop innovative therapeutic strategies to reduce drug resistance. In this review, we proposed a feasible workflow for incorporating AI into tumor drug resistance research, highlighted current AI-driven tumor drug resistance applications, and discussed the opportunities and challenges encountered in the process. Based on a comprehensive literature analysis, we systematically summarized the role of AI in tumor drug resistance research, including drug development, resistance mechanism elucidation, drug sensitivity prediction, combination therapy optimization, resistance phenotype identification, and clinical biomarker discovery. With the continuous advancement of AI technology and rigorous validation of clinical data, AI models are expected to fuel the development of precision oncology by improving efficacy, guiding therapeutic decisions, and optimizing patient prognosis. In summary, by leveraging clinical and omics data, AI models are expected to pioneer new therapy strategies to mitigate tumor drug resistance, improve efficacy and patient survival, and provide novel perspectives and tools for oncology treatment. ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"34 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143862707","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":"Exploring molecular and cellular mechanisms of Pre-Metastatic niche in renal cell carcinoma","authors":"Xiao Zhou, Ruirui Li, Maode Lai, Chong Lai","doi":"10.1186/s12943-025-02315-9","DOIUrl":"https://doi.org/10.1186/s12943-025-02315-9","url":null,"abstract":"Renal cell carcinoma (RCC) is among the most frequently occurring types of cancer, and its metastasis is a major contributor to its elevated mortality. Before the primary tumor metastasizes to secondary or distant organs, it remodels the microenvironment of these sites, creating a pre-metastatic niche (PMN) conducive to the colonization and growth of metastatic tumors. RCC releases a variety of biomolecules that induce angiogenesis, alter vascular permeability, modulate immune cells to create an immunosuppressive microenvironment, affect extracellular matrix remodeling and metabolic reprogramming, and determine the organotropism of metastasis through different signaling pathways. This review summarizes the principal processes and mechanisms underlying the formation of the premetastatic niche in RCC. Additionally, we emphasize the significance and potential of targeting PMNs for the prevention and treatment of tumor metastasis in future therapeutic approaches. Finally, we summarized the currently potential targeted strategies for detecting and treating PMN in RCC and provide a roadmap for further in-depth studies on PMN in RCC.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"2 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143857422","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":"Retraction Note: Dclk1, a tumor stem cell marker, regulates pro-survival signaling and self-renewal of intestinal tumor cells","authors":"Parthasarathy Chandrakesan, Jiannan Yao, Dongfeng Qu, Randal May, Nathaniel Weygant, Yang Ge, Naushad Ali, Sripathi M. Sureban, Modhi Gude, Kenneth Vega, Eddie Bannerman-Menson, Lijun Xia, Michael Bronze, Guangyu An, Courtney W. Houchen","doi":"10.1186/s12943-025-02329-3","DOIUrl":"https://doi.org/10.1186/s12943-025-02329-3","url":null,"abstract":"<p><b>Retraction note:</b><b><i>Mol Cancer</i></b><b>16</b><b>, 30 (2017)</b></p><p>https://doi.org/10.1186/s12943-017-0594-y</p><p>The Editor-in-Chief has retracted this article. After publication, concerns were raised regarding highly similar images in some of the figures, specifically: Fig. 3D Bmi1 and Fig. 3F Hes1 blots appear highly similar; Fig. 3D Lgr 5 and Fig. 3F B-catenin blots appear highly similar; Fig. 3D Musashi1 Fig. 3F NFκBp65 blots appear highly similar; Fig. 7B si-DCLK1 invasion and Fig. 7B si-DCLK1 migration images appear highly similar (with different brightness and contrast); Fig. 7C si-DLCK1 migration and Fig. 7C si-NOTCH1 invasion images appear highly similar (with different brightness and contrast).</p><p>The authors have not been able to address these concerns to the Editor-in-Chief’s satisfaction.</p><p>Nathaniel Weygant, Michael Bronze, and Courtney W. Houchen agree with this retraction. Jiannan Yao does not agree with this retraction. Kenneth Vega as not explicitly stated whether they agree to this retraction. None of the other authors have responded to any correspondence from the Publisher about this retraction.</p><h3>Authors and Affiliations</h3><ol><li><p>Division of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA</p><p>Parthasarathy Chandrakesan, Jiannan Yao, Dongfeng Qu, Randal May, Nathaniel Weygant, Yang Ge, Naushad Ali, Sripathi M. Sureban, Modhi Gude, Kenneth Vega, Michael Bronze & Courtney W. Houchen</p></li><li><p>OU Cancer Institute, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA</p><p>Parthasarathy Chandrakesan, Dongfeng Qu & Courtney W. Houchen</p></li><li><p>Department of Veterans Affairs Medical Center, Oklahoma City, Endocrine, Diabetes, OK, 4Access, USA</p><p>Parthasarathy Chandrakesan, Dongfeng Qu, Randal May, Naushad Ali, Sripathi M. Sureban & Courtney W. Houchen</p></li><li><p>Thyroid center, Oklahoma City, OK, USA</p><p>Modhi Gude</p></li><li><p>Department of Medicine, National Jewish Health, Denver, CO, USA</p><p>Kenneth Vega</p></li><li><p>Oklahoma Medical Research Foundation, Oklahoma City, OK, USA</p><p>Lijun Xia</p></li><li><p>Beijing Chao-Yang Hospital Department of Oncology, Capital Medical University, Beijing, China</p><p>Jiannan Yao, Yang Ge & Guangyu An</p></li><li><p>COARE Biotechnology, Oklahoma City, OK, USA</p><p>Eddie Bannerman-Menson & Courtney W. Houchen</p></li></ol><span>Authors</span><ol><li><span>Parthasarathy Chandrakesan</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Jiannan Yao</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Dongfeng Qu</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"17 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143849607","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":"Transient intracellular expression of PD-L1 and VEGFR2 bispecific nanobody in cancer cells inspires long-term T cell activation and infiltration to combat tumor and inhibit cancer metastasis","authors":"Lei Zhang, Yunfeng Lin, Li Hu, Yanan Wang, Chaohua Hu, Xinyi Shangguan, Shuzhi Tang, Jincan Chen, Ping Hu, Zhe-Sheng Chen, Zun-Fu Ke, Zhuo Chen","doi":"10.1186/s12943-025-02253-6","DOIUrl":"https://doi.org/10.1186/s12943-025-02253-6","url":null,"abstract":"PD-L1, an immune checkpoint inhibitor, and VEGFR2, essential for cancer metastasis, play pivotal roles in tumorigenesis. However, their miniature bispecific intracellular nanobodies for combining check-point blockade and anti-metastasis anticancer therapy remain underexplored. The intrabodies were developed using gene cloning technology. Specificity of the intrabodies was testified using Western blot, co-immunoprecipitation (co-IP) analysis, antibody competitive binding assay, flow cytometry analysis, etc. Checkpoint blockade was demonstrated using antibody-antigen competitive binding assay. Cancer cell migration was determined using scratch assay. Combined anti-cancer therapeutic efficacy of FAP1V2 was determined in vivo of mice models. The PD-1hi immune cells, TCR βhi and CD25hi T-cells were analyzed by flow cytometry, and cancer cell metastasis was performed using immune-fluorescence analysis on lung and liver tissues. Transcriptome analysis was performed to explore signaling pathways associated with the enhanced anticancer efficiency. Bispecific intrabody FAP1V2 fused with antibody VH regions, was successfully developed and verified with its ability to target and block human and mouse PD-L1 and VEGFR2, inhibiting cancer cell binding to PD-1 and reducing their migratory capacity. Compared to the other treatment, two-rounds of transient FAP1V2 expression in LLC cells in experimental mice models achieved remarkable tumor inhibition, which brought about complete immune inhibition on growth of secondary-round of LLC tumor in 1/6 of the tested mice, inspired long-term activation of TCR βhi T cells and increased their infiltration to tumors, inhibited the emergence of PD-1hi immune cells, indicating prevented T cell depletion. The elevated CD25 expression also supported the success in enhancing immune response reported by elevated T cell activity in spleen. Transcriptome analysis identified critical intracellular pathways regulated by the concurrent blockade of PD-L1 and VEGFR2. PD-L1 and VEGFR2- bispecific VH intracellular nanobody was highly biocompatible and showed the potential for combined anti-cancer therapy through long-term immune activation mediated by PD-L1/PD-1 checkpoint blockade and anti-metastasis mediated by VEGFR2 blockade.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"4 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143849604","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":"ADAR1-high tumor-associated macrophages induce drug resistance and are therapeutic targets in colorectal cancer","authors":"Hibiki Umeda, Kunitoshi Shigeyasu, Toshiaki Takahashi, Kazuya Moriwake, Yoshitaka Kondo, Kazuhiro Yoshida, Sho Takeda, Shuya Yano, Yuki Matsumi, Hiroyuki Kishimoto, Tomokazu Fuji, Kazuya Yasui, Hideki Yamamoto, Kosei Takagi, Masashi Kayano, Hiroyuki Michiue, Keiichiro Nakamura, Yoshiko Mori, Fuminori Teraishi, Hiroshi Tazawa, Yuzo Umeda, Shunsuke Kagawa, Ajay Goel, Toshiyoshi Fujiwara","doi":"10.1186/s12943-025-02312-y","DOIUrl":"https://doi.org/10.1186/s12943-025-02312-y","url":null,"abstract":"Colorectal cancer (CRC) is considered the third most common type of cancer worldwide. Tumor-associated macrophages (TAMs) have been shown to promote drug resistance. Adenosine-to-inosine RNA-editing, as regulated by adenosine deaminase acting on RNA (ADAR), is a process that induces the posttranscriptional modification of critical oncogenes. The aim of this study is to determine whether the signals from cancer cells would induce RNA-editing in macrophages. The effects of RNA-editing on phenotypes in macrophages were analyzed using clinical samples and in vitro and in vivo models. The intensity of the RNA-editing enzyme ADAR1 (Adenosine deaminase acting on RNA 1) in cancer and mononuclear cells indicated a strong positive correlation between the nucleus and cytoplasm. The ADAR1-positive mononuclear cells were positive for CD68 and CD163, a marker for M2 macrophages. Cancer cells transport pro-inflammatory cytokines or ADAR1 protein directly to macrophages via the exosomes, promoting RNA-editing in AZIN1 (Antizyme Inhibitor 1) and GLI1 (Glioma-Associated Oncogene Homolog 1) and resulting in M2 macrophage polarization. GLI1 RNA-editing in the macrophages induced by cancer cells promotes the secretion of SPP1, which is supplied to the cancer cells. This activates the NFκB pathway in cancer cells, promoting oxaliplatin resistance. When the JAK inhibitors were administered, oncogenic RNA-editing in the macrophages was suppressed. This altered the macrophage polarization from M2 to M1 and decreased oxaliplatin resistance in cancer cells. This study revealed that ADAR1-high TAMs are crucial in regulating drug resistance in CRC and that targeting ADAR1 in TAMs could be a promising treatment approach for overcoming drug resistance in CRC.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"108 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836919","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: Targeting SOST using a small‑molecule compound retards breast cancer bone metastasis","authors":"Lisha Sun, Yixiao Zhang, Guanglei Chen, Yaoting Ji, Qingtian Ma, Xinbo Qiao, Sijin Wu, Lin Zhou, Jiawen Bu, Xudong Zhu, Xiaoying Zhang, Xiaofan Jiang, Chao Liu, Xinnan Li, Yang Liu, Yongliang Yang, Caigang Liu","doi":"10.1186/s12943-025-02322-w","DOIUrl":"https://doi.org/10.1186/s12943-025-02322-w","url":null,"abstract":"<p><b>Correction:</b> <b><i>Mol Cancer</i></b> <b>21</b><b>, 228 (2022)</b></p><p><b>https://doi.org/10.1186/s12943-022-01697-4</b></p><p>Following publication of the original article [1], the authors dentified an inadvertent image duplication in the supplementary Figure S2-C which occurred during the figure preparation process and wish to formally request an erratum to rectify this issue. The updated Figure S2-C can be downloaded from the link provided in the Additional file 1 below.</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Sun L, Zhang Y, Chen G, et al. Targeting SOST using a small-molecule compound retards breast cancer bone metastasis. Mol Cancer. 2022;21:228. https://doi.org/10.1186/s12943-022-01697-4.</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>Lisha Sun, Yixiao Zhang, Guanglei Chen and Yaoting Ji contributed equallyto this work.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>Department of Oncology, Innovative Cancer Drug Research and Engineering Center of Liaoning Province, Cancer Stem Cell and Translation Medicine Lab, Shengjing Hospital of China Medical University, Shenyang, China</p><p>Lisha Sun, Yixiao Zhang, Guanglei Chen, Qingtian Ma, Xinbo Qiao, Jiawen Bu, Xudong Zhu, Xiaoying Zhang, Xiaofan Jiang, Chao Liu, Xinnan Li & Caigang Liu</p></li><li><p>Department of Urology Surgery, Shengjing Hospital of China Medical University, Shenyang, China</p><p>Yixiao Zhang</p></li><li><p>The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei‑MOST) and Key Laboratory for Oral Biomedicine of Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China</p><p>Yaoting Ji</p></li><li><p>Dalian Institute of Chemical Physics, Chinese Academy of Science, Dalian, China</p><p>Sijin Wu</p></li><li><p>Key Laboratory of Structure‑Based Drug Design & Discovery of Ministry of Education, Shenyang Pharmaceutical University, Shenyang, China</p><p>Lin Zhou & Yang Liu</p></li><li><p>School of Bioengineering, Dalian University of Technology, Dalian, China</p><p>Yongliang Yang</p></li></ol><span>Authors</span><ol><li><span>Lisha Sun</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yixiao Zhang</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Guanglei Chen</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yaoting Ji</span>View author publications<p><span>You can also sear","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"26 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836854","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":"Lung-specific metastasis: the coevolution of tumor cells and lung microenvironment","authors":"Guixiu Xiao, Xinmin Wang, Zihan Xu, Yanyang Liu, Jing Jing","doi":"10.1186/s12943-025-02318-6","DOIUrl":"https://doi.org/10.1186/s12943-025-02318-6","url":null,"abstract":"The vast majority of cancer-related deaths are attributed to metastasis. The lung, being a common site for cancer metastasis, is highly prone to being a target for multiple cancer types and causes a heavy disease burden. Accumulating evidence has demonstrated that tumor metastasis necessitates continuous interactions between tumor cells and distant metastatic niches. Nevertheless, a comprehensive elucidation of the underlying mechanisms governing lung-specific metastasis still poses a formidable challenge. In this review, we depict the lung susceptibility and the molecular profiles of tumors with the potential for lung metastasis. Under the conceptual framework of “Reciprocal Tumor-Lung Metastatic Symbiosis” (RTLMS), we mechanistically delineate the bidirectional regulatory dynamics and coevolutionary adaptation between tumor cells and distal pulmonary niches during lung-specific metastasis, including the induction of pre-metastatic-niches, positive responses of the lung, tumor colonization, dormancy, and reawakening. An enhanced understanding of the latest mechanisms is essential for developing targeted strategies to counteract lung-specific metastasis.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"2 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836918","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}