Cellular & Molecular Biology Letters最新文献

{"title":"Rho-GTPases subfamily: cellular defectors orchestrating viral infection.","authors":"Beibei Zhang, Shuli Li, Juntao Ding, Jingxia Guo, Zhenghai Ma, Hong Duan","doi":"10.1186/s11658-025-00722-w","DOIUrl":"https://doi.org/10.1186/s11658-025-00722-w","url":null,"abstract":"<p><p>Ras homolog gene family-guanosine triphosphatases (Rho-GTPases), key molecular switches regulating cytoskeletal dynamics and cellular signaling, play a pivotal role in viral infections by modulating critical processes such as viral entry, replication, and release. This review elucidates the intricate mechanisms through which Rho-GTPases, via interactions with guanine nucleotide exchange factors (GEFs), GTPase-activating proteins (GAPs), and other signaling pathways, including the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), rat sarcoma (Ras), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways, facilitate viral pathogenesis. Specific viruses, such as influenza A virus (IAV), herpesviruses, human immunodeficiency virus (HIV), and respiratory syncytial virus (RSV), exploit Rho-GTPase-mediated cytoskeletal reorganization to enhance infectivity. For example, Rho-GTPases promote actin remodeling and membrane fusion, which are essential for viral entry and intracellular transport. Furthermore, Rho-GTPases modulate immune responses, often suppressing antiviral defenses to favor viral replication. Despite these insights, the molecular mechanisms underlying Rho-GTPase regulation during viral infections remain incompletely understood. Future research should focus on delineating the precise roles of Rho-GTPases in distinct viral life cycles, uncovering novel regulatory mechanisms, and developing targeted antiviral therapies that selectively inhibit Rho-GTPase signaling without compromising host cell functions. Such advancements could pave the way for broad-spectrum antiviral strategies, particularly against viruses that heavily rely on cytoskeletal manipulation for infection.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":"30 1","pages":"55"},"PeriodicalIF":9.2,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12049043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143962604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential of autophagy in subretinal fibrosis in neovascular age-related macular degeneration.","authors":"Janusz Blasiak, Elzbieta Pawlowska, Hanna Helotera, Maksim Ionov, Marcin Derwich, Kai Kaarniranta","doi":"10.1186/s11658-025-00732-8","DOIUrl":"https://doi.org/10.1186/s11658-025-00732-8","url":null,"abstract":"<p><p>Age-related macular degeneration (AMD) is an eye disease that can lead to legal blindness and vision loss. In its advanced stages, it is classified into dry and neovascular AMD. In neovascular AMD, the formation of new blood vessels disrupts the structure of the retina and induces an inflammatory response. Treatment for neovascular AMD involves antibodies and fusion proteins targeting vascular endothelial growth factor A (VEGFA) and its receptors to inhibit neovascularization and slow vision loss. However, a fraction of patients with neovascular AMD do not respond to therapy. Many of these patients exhibit a subretinal fibrotic scar. Thus, retinal fibrosis may contribute to resistance against anti-VEGFA therapy and the cause of irreversible vision loss in neovascular AMD patients. Retinal pigment epithelium cells, choroidal fibroblasts, and retinal glial cells are crucial in the development of the fibrotic scar as they can undergo a mesenchymal transition mediated by transforming growth factor beta and other molecules, leading to their transdifferentiation into myofibroblasts, which are key players in subretinal fibrosis. Autophagy, a process that removes cellular debris and contributes to the pathogenesis of AMD, regardless of its type, may be stimulated by epithelial-mesenchymal transition and later inhibited. The mesenchymal transition of retinal cells and the dysfunction of the extracellular matrix-the two main aspects of fibrotic scar formation-are associated with impaired autophagy. Nonetheless, the causal relationship between autophagy and subretinal fibrosis remains unknown. This narrative/perspective review presents information on neovascular AMD, subretinal fibrosis, and autophagy, arguing that impaired autophagy may be significant for fibrosis-related resistance to anti-VEGFA therapy in neovascular AMD.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":"30 1","pages":"54"},"PeriodicalIF":9.2,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12044759/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cdkn1a silencing restores myoblast differentiation by inducing selective apoptosis in senescent cells.","authors":"Sujin Kim, Bonsang Gu, Chan-Young So, Keren Esther Kristina Mantik, Seung-Hyun Jung, Sohee Moon, Dong-Ho Park, Hyo-Bum Kwak, Jinkyung Cho, Eun-Jeong Cho, Jae-Seon Lee, Ju-Hee Kang","doi":"10.1186/s11658-025-00731-9","DOIUrl":"https://doi.org/10.1186/s11658-025-00731-9","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenia, characterized by a progressive loss of skeletal muscle mass and function, is associated with the accumulation of senescent muscle stem cells, which impair muscle regeneration and contributes to the decline in muscle health. Cdkn1a, which encodes p21, is a well-known marker of cellular senescence. However, it remains unclear whether p21 inhibition eliminates senescent myoblasts and restores the differentiation capacity.</p><p><strong>Methods: </strong>We performed transcriptomic analysis to identify genes related to aging-induced sarcopenia using 21 month-old Sprague-Dawley rats. To investigate the specific role of Cdkn1a gene in muscle aging, we used an in vitro model of ceramide-induced senescence in myoblasts, which was verified by the upregulation of p21 and increased senescence-associated beta-galactosidase (SA-β-gal) staining. To inhibit p21, we treated myoblasts with small interfering RNA (siRNA) targeting Cdkn1a. Using fluorescence-activated cell sorting, we separated subpopulations of cells with high or low caspase 3/7 activity. Protein expression related to myogenesis, muscle atrophy, protein synthesis, and apoptosis were quantified by western blotting.</p><p><strong>Results: </strong>In our transcriptomic analysis, we identified Cdkn1a as an upregulated gene in both the soleus and white gastrocnemius muscles of aged rats, among 36 commonly upregulated genes. The upregulation of Cdkn1a appears to be linked to mitochondrial dysfunction and cellular senescence, underscoring its significance in sarcopenia pathogenesis. C2-ceramide treatment effectively induced senescence, as evidenced by increased p21 expression, enhanced SA-β-gal staining, decreased myogenesis, and increased apoptosis. Knockdown of p21 in ceramide-treated myoblasts significantly reduced SA-β-gal-positive cells, restored cell proliferation, reduced the expression of senescence-associated cytokines (i.e., interleukin (IL)-6 and tumor necrosis factor (TNF)-α), and selectively induced apoptosis in the senescent cell population, demonstrating a senolytic effect. Notably, p21 inhibition also improved differentiation of myoblasts into myotubes, as indicated by increased myosin heavy chain expression and improvements in myotube diameter and fusion index.</p><p><strong>Conclusions: </strong>Our data suggest that p21 inhibition selectively eliminates senescent cells while simultaneously enhancing the regenerative capacity of healthy myoblasts, which may combine to improve muscle regeneration and promote myogenesis, ultimately improving muscle health and function in aged individuals.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":"30 1","pages":"53"},"PeriodicalIF":9.2,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12042464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Etoposide-induced protein 2.4 homolog promotes argininosuccinate synthase 1 and cancer cell survival upon arginine deprivation.","authors":"Vu T A Vo, Le Nhat Tran, Thu Thanh Bui, Han-Woong Lee, Yangsik Jeong","doi":"10.1186/s11658-025-00726-6","DOIUrl":"https://doi.org/10.1186/s11658-025-00726-6","url":null,"abstract":"<p><strong>Background: </strong>Arginine auxotrophy has been reported in a subset of cancers with inherently defective de novo arginine synthesis. However, the use of arginine deprivation therapy seems to be unequally effective, partially owing to the resistance acquired by cancer cells. Study of underlying factors involved in this response thus becomes of utmost importance. Meanwhile, the function of etoposide-induced 2.4 homolog (EI24) in cancer metabolism, and specifically in arginine metabolism, remains unknown.</p><p><strong>Methods: </strong>EI24 was overexpressed in cancer cells using a doxycycline-inducible system or adenovirus transduction, while siRNA was used to knockdown EI24. Amino acid(s) deprivation medium was exploited with a cell viability assay to check the reliance of cancer cell survival on arginine. Protein expression and activation were examined through western blot and co-immunoprecipitation blot. Furthermore, global and specific protein translation were assessed through the SUnSET assay and polysome fractionation analysis. Gene expression and arginine level were downloaded from public cancer datasets for in silico validation including gene set enrichment and survival analysis to objectively evaluate the association between EI24 and arginine metabolism.</p><p><strong>Results: </strong>EI24 promoted cancer survival under arginine starvation. Mechanistically, EI24 replenished translation of argininosuccinate synthase 1 (ASS1) by inducing the inactive S-nitrosylated form of phosphatase and tensin homolog (PTEN), leading to release of the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) axis. This tumor-promoting action of EI24 could be found in multiple ASS1-deficient cancer cells regardless of p53 status. Furthermore, expression of EI24 was linked to enrichment of arginine metabolism pathway as well as poor survival of patients with cancer across various cancer types, suggesting its role in cancer resistance to arginine deprivation.</p><p><strong>Conclusions: </strong>This study is the first to report the role of EI24 in promoting cancer survival via translational regulation of the metabolic enzyme ASS1, thus paving a route for further investigation into the link between EI24 and cancer metabolism.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":"30 1","pages":"52"},"PeriodicalIF":9.2,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12008907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Silibinin suppresses epithelial-mesenchymal transition in human non-small cell lung cancer cells by restraining RHBDD1.","authors":"Suyan Xu, Hongyan Zhang, Aifeng Wang, Yongcheng Ma, Yuan Gan, Guofeng Li","doi":"10.1186/s11658-025-00728-4","DOIUrl":"https://doi.org/10.1186/s11658-025-00728-4","url":null,"abstract":"","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":"30 1","pages":"50"},"PeriodicalIF":9.2,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12008881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the role of gut microbiota modulation in the long-term therapeutic benefits of early MSC transplantation in MRL/lpr mice.","authors":"Quanren Pan, Fengbiao Guo, Jiaxuan Chen, Haimin Huang, Yanyan Huang, Shuzhen Liao, Zengzhi Xiao, Xi Wang, Liuyong You, Lawei Yang, Xuemei Huang, Haiyan Xiao, Hua-Feng Liu, Qingjun Pan","doi":"10.1186/s11658-025-00716-8","DOIUrl":"https://doi.org/10.1186/s11658-025-00716-8","url":null,"abstract":"<p><strong>Background: </strong>Systemic lupus erythematosus (SLE), influenced by gut microbiota dysbiosis, is characterized by autoimmune and inflammatory responses. Human umbilical cord-derived mesenchymal stem cell (hUC-MSC) transplantation is an effective and safe treatment for refractory or severe SLE; however, the long-term efficacy and mechanisms of early hUC-MSC therapeutic benefits in SLE need further investigation.</p><p><strong>Methods: </strong>Here, lupus-prone MRL/MpJ-Fas^lpr (MRL/lpr) mice were divided into three groups: the control (Ctrl) group received saline injections, while the MSC and MSC-fecal microbiota transplantation (FMT) groups received early hUC-MSC transplants at weeks 6, 8, and 10. The MSC-FMT group also underwent FMT from the Ctrl group between weeks 9 and 13.</p><p><strong>Results: </strong>Our results showed that early MSC treatment extended therapeutic effects up to 12 weeks, reducing autoantibodies, proinflammatory cytokines, B cells, and improving lupus nephritis. It also modulated the gut microbiota, increasing the abundance of beneficial bacteria, such as Lactobacillus johnsonii and Romboutsia ilealis, which led to higher levels of plasma tryptophan and butyrate metabolites. These metabolites activate the aryl hydrocarbon receptor (AHR), upregulate the Cyp1a1 and Cyp1b1 gene, enhance the zonula occludens 1 (ZO-1) protein, promote intestinal repair, and mitigate SLE progression. Notably, FMT from lupus mice significantly reversed hUC-MSC benefits, suggesting that the modulation of the gut microbiota plays a crucial role in the therapeutic response observed in MRL/lpr mice.</p><p><strong>Conclusions: </strong>This research innovatively explores the early therapeutic window for MSCs in SLE, highlighting the partial mechanisms through which hUC-MSCs modulate the gut microbiota-tryptophan-AHR axis, thereby ameliorating SLE symptoms.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":"30 1","pages":"49"},"PeriodicalIF":9.2,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12007202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: MicroRNA-582-3p negatively regulates cell proliferation and cell cycle progression in acute myeloid leukemia by targeting cyclin B2.","authors":"Haixia Li, Xuefei Tian, Paoqiu Wang, Mao Huang, Ronghua Xu, Tian Nie","doi":"10.1186/s11658-025-00729-3","DOIUrl":"https://doi.org/10.1186/s11658-025-00729-3","url":null,"abstract":"","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":"30 1","pages":"51"},"PeriodicalIF":9.2,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12008909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating innate lymphoid cells are dysregulated in patients with prostate cancer.","authors":"Daniela Claudia Maresca, Evelina La Civita, Benedetta Romano, Maria Rosaria Ambrosio, Fabio Somma, Tania Wyss, Bernardo Rocco, Valentina Rubino, Luigi Cari, Philippe Krebs, Antonio Rodriguez-Calero, Matteo Ferro, Sara Trabanelli, Camilla Jandus, Felice Crocetto, Angela Ianaro, Daniela Terracciano, Giuseppe Ercolano","doi":"10.1186/s11658-025-00725-7","DOIUrl":"https://doi.org/10.1186/s11658-025-00725-7","url":null,"abstract":"<p><strong>Background: </strong>Prostate cancer (PCa) is the second most common cancer affecting men globally, especially those aged 50 years and above. Despite substantial progress in terms of both prognosis and therapy, PCa remains a significant health concern, necessitating the identification of novel therapeutic targets. Innate lymphoid cells (ILCs) have emerged as critical modulators of tumor immunity, exhibiting both pro- and antitumoral effects. However, little is known yet about their contribution in PCa. This study investigated the phenotypic and functional profiles of ILC subsets in the peripheral blood mononuclear cells (PBMCs) of patients with PCa stratified by Gleason score.</p><p><strong>Methods: </strong>PBMCs were isolated by Lymphoprep. ILC frequency and activity were evaluated by flow cytometry. The levels of ILC-activating cytokines were analyzed by multiplex assay in the serum of healthy donors (HDs) and patients with PCa. To evaluate the crosstalk between ILC2s and cancer cells, PC3 and DU145 human PCa cell lines were used.</p><p><strong>Results: </strong>We found a stage-dependent increase in the protumoral ILC2 frequency and a concurrent decrease in antitumoral ILC1s in patients with PCa compared with healthy controls. Interestingly, the frequency of ILC2s was higher in patients with elevated prostate-specific antigen (PSA) values, suggesting their potential as molecular predictor for defining the risk category of patients with PCa at diagnosis. Importantly, patients with PCa exhibited hyperactivated ILC2s, characterized by elevated interleukin (IL)-13 and IL-5 production, while ILC1s displayed reduced tumor necrosis factor (TNF)-α and interferon (IFN)-γ secretion. Furthermore, serum levels of ILC2-activating cytokines IL-33, IL-18, and prostaglandin D2 (PGD2) were elevated in patients with PCa. In vitro co-culture experiments demonstrated that PCa cell lines, capable of secreting these cytokines, could directly enhance ILC2 activity. Likewise, ILC2-derived IL-13 promoted PCa cell migration and invasion.</p><p><strong>Conclusions: </strong>Collectively, our findings highlight a dysregulated ILC profile in PCa, characterized by ILC2 dominance and heightened activity at the expense of ILC1s, suggesting both ILC1s and ILC2s as potential therapeutic targets for PCa treatment.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":"30 1","pages":"48"},"PeriodicalIF":9.2,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12007220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of USP7 in the regulation of tolerogenic dendritic cell function in type 1 diabetes.","authors":"Farhan Ullah Khan, Puregmaa Khongorzul, Denis Gris, Abdelaziz Amrani","doi":"10.1186/s11658-025-00727-5","DOIUrl":"https://doi.org/10.1186/s11658-025-00727-5","url":null,"abstract":"<p><strong>Background: </strong>Tolerogenic dendritic cells (toDCs) are critical for maintaining immune homeostasis and preventing autoimmune disease development, such as type 1 diabetes (T1D). We have previously shown that DCs of non-obese diabetic (NOD) mice expressing active Stat5b (Stat5b-CA.DCs) acquire toDCs signature and protect against diabetes. However, the mechanisms involved in reprogramming DCs to adopt tolerogenic or immunogenic signatures are not fully known. This study investigates for the first time the role of USP7 in DC-mediated immune regulation in T1D using a transgenic NOD mouse model expressing an active form of Stat5b (NOD.Stat5b-CA).</p><p><strong>Methods: </strong>Splenic DCs were purified from diabetes-prone NOD mice and diabetes-resistant NOD.Stat5b-CA transgenic mice and their tolerogenic and immunogenic phenotypes were analyzed by FACS. Their pro-and anti-inflammatory cytokine patterns, IRF4, IRF8, de-ubiquitin ligase USP7, and methyltransferase Ezh2 expression were assessed by FACS and Western blot. Moreover, the impact of USP7 inhibition in DCs on Th1/Th2/Th17 and Treg and diabetes onset was assessed using an in vivo DC-based transfer model.</p><p><strong>Results: </strong>In this study, we found that splenic Stat5b-CA.DCs expressed high levels of USP7, Ezh2, and PD-L-1/2 and contained a higher proportion of tolerogenic conventional DC2 (cDC2) subsets than immunogenic cDC1 compared to NOD mice DCs. We also found that the USP7 blockade increased Stat5b-CA.DCs maturation and proinflammatory cytokines production while decreasing anti-inflammatory cytokines and PD-L1 and PD-L2 expressions. Mechanistically, USP7 blockade in Stat5-CA.DCs promoted cDC1 over cDC2 subsets by increasing IRF8 expression in an Ezh2-dependent manner and decreasing IRF4 expression independently of Ezh2. USP7 blockade also increased Stat5b-CA.DC capacity to promote Th17 and to restrain Th2 and Treg cells. Importantly, the capacity of Stat5b-CA.DCs to protect NOD mice from diabetes were lost when treated with USP7 inhibitor.</p><p><strong>Conclusions: </strong>Our findings underscore the role of the USP7/Ezh2 axis in maintaining tolerogenic DC functions that are required to tailor adaptive immune response and diabetes protection in NOD mice.</p>","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":"30 1","pages":"47"},"PeriodicalIF":9.2,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12004606/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143962875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: PAK4, a target of miR-9-5p, promotes cell proliferation and inhibits apoptosis in colorectal cancer.","authors":"Meihua Wang, Qianqian Gao, Yufang Chen, Ziyan Li, Lingping Yue, Yun Cao","doi":"10.1186/s11658-025-00730-w","DOIUrl":"https://doi.org/10.1186/s11658-025-00730-w","url":null,"abstract":"","PeriodicalId":9688,"journal":{"name":"Cellular & Molecular Biology Letters","volume":"30 1","pages":"46"},"PeriodicalIF":9.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12004659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}