Experimental cell research最新文献

Lactate promotes the epithelial-mesenchymal transition of liver cancer cells via TWIST1 lactylation.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-22 DOI: 10.1016/j.yexcr.2025.114474

Wang Huimin, Wu Xin, Yu Shan, Zhang Junwang, Wen Jing, Wang Yuan, Liu Qingtong, Li Xiaohui, Yao Jia, Yuan Lili

{"title":"Lactate promotes the epithelial-mesenchymal transition of liver cancer cells via TWIST1 lactylation.","authors":"Wang Huimin, Wu Xin, Yu Shan, Zhang Junwang, Wen Jing, Wang Yuan, Liu Qingtong, Li Xiaohui, Yao Jia, Yuan Lili","doi":"10.1016/j.yexcr.2025.114474","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114474","url":null,"abstract":"<p><p>Elevated lactate levels increase the risk of liver cancer progression. However, the mechanisms by which lactate promotes liver cancer progression remain poorly understood. Epithelial-mesenchymal transition (EMT), characterized by the loss of epithelial cells polarity and cell-cell adhesion, leading to the acquisition of mesenchymal-like phenotypes, is widely recognized as a key contributor to liver cancer progression. TWIST1 (Twist Family BHLH Transcription Factor 1) plays a central role in inducing EMT. Here, we investigated the role of lactate in promoting EMT in liver cancer and the underlying regulatory mechanisms. High levels of lactate significantly promoted EMT progression in liver cancer cells. Mechanistically, lactate-induced lactylation of TWIST1 in vivo and in vitro. Mutation assay confirmed that Lysine 33 (K33) is the major site of TWIST1 lactylation. Moreover, cell fractionation & luciferase reporter assay results identified that TWIST1-K33R mutant impaired the EMT process via inhibiting nuclear import and the transcriptional activity. Thus, our findings provide novel insights into the regulatory role of lactate in EMT in liver cancer pathogenesis. Additionally, targeting of lactate-driven lactylation of TWIST1 may boost the therapeutic strategy for liver cancer.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114474"},"PeriodicalIF":3.3,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanical stretch promotes the migration of mesenchymal stem cells via Piezo1/F-actin/YAP axis

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-21 DOI: 10.1016/j.yexcr.2025.114461

Ning Ma , Lei Huang , Qianxu Zhou , Xiaomei Zhang , Qing Luo , Guanbin Song

{"title":"Mechanical stretch promotes the migration of mesenchymal stem cells via Piezo1/F-actin/YAP axis","authors":"Ning Ma , Lei Huang , Qianxu Zhou , Xiaomei Zhang , Qing Luo , Guanbin Song","doi":"10.1016/j.yexcr.2025.114461","DOIUrl":"10.1016/j.yexcr.2025.114461","url":null,"abstract":"<div><div>Mesenchymal stem cells (MSCs) have self-renewal ability and the potential for multi-directional differentiation, and their clinical application has promising prospects, but improving the migration ability of MSCs <em>in vivo</em> is one of the challenges. We previously determined mechanical stretch at 1 Hz with 10 % strain for 8 h can significantly promote MSC migration, however, the molecular mechanism remains poorly understood. Here, we reported that the expression and activity of yes-associated protein (YAP) are upregulated after mechanical stretch. As a classical inhibitor of the YAP-TEAD activity and YAP protein, the treatment of verteporfin (VP) suppressed mechanical stretch-promoted MSC migration. We also observed F-actin polymerization after mechanical stretch. Next, we used Latrunculin A (Lat A), the most widely used reagent to depolymerize actin filaments, to treat MSCs and we found that Lat A treatment inhibits MSC migration by suppressing YAP expression and activity. In addition, the protein expression of Piezo1 was also upregulated after mechanical stretch. Knockdown of Piezo1 suppressed mechanical stretch-promoted MSC migration by restraining F-actin polymerization. Together, these findings demonstrate the role of Piezo1/F-actin/YAP signaling pathway in MSC migration under mechanical stretch, providing new experimental evidence for an in-depth understanding the mechanobiological mechanism of MSC migration.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114461"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mapping the initial effects of carcinogen-induced oncogenic transformation in the mouse bladder 绘制小鼠膀胱中致癌物质诱导的致癌转化的初始效应图

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-21 DOI: 10.1016/j.yexcr.2025.114452

Md. Kaykobad Hossain , Lucas Unger , Ulrik Larsen , Altanchimeg Altankhuyag , Thomas Aga Legøy , Joao A. Paulo , Heidrun Vethe , Luiza Ghila

{"title":"Mapping the initial effects of carcinogen-induced oncogenic transformation in the mouse bladder","authors":"Md. Kaykobad Hossain , Lucas Unger , Ulrik Larsen , Altanchimeg Altankhuyag , Thomas Aga Legøy , Joao A. Paulo , Heidrun Vethe , Luiza Ghila","doi":"10.1016/j.yexcr.2025.114452","DOIUrl":"10.1016/j.yexcr.2025.114452","url":null,"abstract":"<div><div>Characterizing the initial stages of oncogenic transformation allows the identification of tumor-promoting processes before the inherent clonal selection of the aggressive clones. Here, we used global proteomics, genetic cell tracing, and immunofluorescence to dynamically map the very early stages of cancer initiation in a mouse model of bladder cancer. We observed a very rapid and incremental proteome dysregulation, with changes in the energy metabolism, proliferation and immune signatures dominating the landscape. The changes in the lipid metabolism were immediate and defined by an increase fatty acid metabolism and lipid transport, followed by the activation of the immune landscape. Alongside the changes in the immune signature and lipid metabolism, we also mapped a clear increase in the cell cycle-related pathways and proliferation. Proliferation was mainly restricted to the basal epithelial layer rapidly leading to urothelium thickening, despite the progressive loss of the superficial layer. Moreover, we observed a tilt in the energy balance towards increased glucose metabolism, probably characterizing cells of the tumor microenvironment. All of the observed proteome signature changes were persistent, being retained and sometimes intensified or diversified along the timeline. The signatures observed in this pilot suggest these processes as potentially targetable drivers of the future neoplastic transformations in the bladder.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114452"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Activated NETosis of bone marrow neutrophils up-regulates macrophage osteoclastogenesis via cGAS-STING/AKT2 pathway to promote osteoporosis.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-21 DOI: 10.1016/j.yexcr.2025.114477

Yutong Guo, Hanzhang Zhou, Yixiang Wang, Yan Gu

引用次数: 0

microRNA-30c attenuates contrast-induced acute kidney injury by reducing renal tubular epithelial cell apoptosis via targeting SOCS1.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-20 DOI: 10.1016/j.yexcr.2025.114456

Long Peng, Yanting Luo, Fang Tan, Qian Chen, Jiafu Wang, Xiaolan Ouyang, Bingyuan Wu, Xixiang Tang, Suhua Li

{"title":"microRNA-30c attenuates contrast-induced acute kidney injury by reducing renal tubular epithelial cell apoptosis via targeting SOCS1.","authors":"Long Peng, Yanting Luo, Fang Tan, Qian Chen, Jiafu Wang, Xiaolan Ouyang, Bingyuan Wu, Xixiang Tang, Suhua Li","doi":"10.1016/j.yexcr.2025.114456","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114456","url":null,"abstract":"<p><p>Contrast-induced acute kidney injury (CIAKI) is a common complication after contrast media administration. Growing evidences implicate microRNA (miR)-30c has a key role in renal diseases. This study aimed to investigate the role and mechanism of miR-30c in CIAKI. CIAKI rat models were established using tail vein injection of omnipaque. MiR-30c was significantly downregulated in CIAKI models both in vivo and in vitro, concomitant with increased cell apoptosis and deteriorated renal injury. Meanwhile, the cell apoptosis, renal dysfunction and renal injury under contrast exposure were alleviated after overexpression of miR-30c. Mechanistically, we demonstrated that miR-30c directly targeted SOCS1, whose downregulation reduced contrast-induced HK-2 cell apoptosis. Furthermore, the upregulation of SOCS1 abolish the protective effect of the overexpression of miR-30c on contrast-induced cell apoptosis. In summary, overexpression of miR-30c inhibited renal tubular epithelial cell apoptosis and mitigated CIAKI via inhibiting the gene of SOCS1.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114456"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mutation in α-Syn impairs insulin signaling pathway and induces neuroinflammation in the α-Syn Parkinson's Drosophila model.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-20 DOI: 10.1016/j.yexcr.2025.114460

Pooja Rai, Rakesh Kumar

{"title":"Mutation in α-Syn impairs insulin signaling pathway and induces neuroinflammation in the α-Syn Parkinson's Drosophila model.","authors":"Pooja Rai, Rakesh Kumar","doi":"10.1016/j.yexcr.2025.114460","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114460","url":null,"abstract":"<p><p>Mutations in the alpha-synuclein (α-Syn) gene have been causally linked to familial Parkinson's disease (PD). PD is primarily characterized by the progressive loss of dopaminergic neurons in the substantia nigra region of the brain. Α-Syn plays a pivotal role in the formation of Lewy bodies (LB), serving as a prominent pathological marker in PD. Growing evidence has illuminated the involvement of the insulin signaling pathway dysfunction in various neurodegenerative models. This study set out to explore how α-Syn influences the insulin signaling pathway and the overall lifespan of fruit flies afflicted with Parkinson's disease. It has been established that the α-Syn gene affects mitochondrial function, with mutations leading to mitochondrial impairments and increased oxidative stress, which ultimately contributes to the death of dopaminergic neurons.The impairment of mitochondrial function disrupts metabolism and exerts an adverse influence on the insulin signaling pathway. Furthermore, the unfolded protein response of the endoplasmic reticulum (ER) are investigated and observed a decrease in the expression of PERK (Protein kinase R-like ER kinase) during ER stress. These findings confirmed the intricate interplay between the insulin signaling pathway and the activation of the \"PERK-ER\" stress pathway. However, the degeneration of neurons triggers a neuroinflammatory response, which are found to be mitigated by the improvement of insulin signaling and the \"PERK-ER\" stress-related pathway. This study's results shed light on the novel regulatory role of PERK within the insulin signaling pathway and suggest its potential as a therapeutic candidate for modulating neuroinflammation in the context of α-Syn -associated Parkinson's Disease pathology.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114460"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Maternal protein restriction impairs intestinal morphophysiology and antioxidant system in young male offspring rats 母体蛋白质限制会损害幼年雄性后代大鼠的肠道形态生理学和抗氧化系统

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-20 DOI: 10.1016/j.yexcr.2025.114464

Isabela Baptista Leal dos Santos , Matheus Naia Fioretto , Miguel Silingardi Jorge , Luísa Annibal Barata , Isabelle Tenori Ribeiro , André Matheus Leandro Franzolin , Erick Guilherme Stoppa , Renato Mattos , Luiz Marcos Frediane Portela , Maycon Tavares Emílio Silva , Sérgio Alexandre Alcântara dos Santos , José Ricardo de Arruda Miranda , Clélia Akiko Hiruma Lima , Luis Antonio Justulin

{"title":"Maternal protein restriction impairs intestinal morphophysiology and antioxidant system in young male offspring rats","authors":"Isabela Baptista Leal dos Santos , Matheus Naia Fioretto , Miguel Silingardi Jorge , Luísa Annibal Barata , Isabelle Tenori Ribeiro , André Matheus Leandro Franzolin , Erick Guilherme Stoppa , Renato Mattos , Luiz Marcos Frediane Portela , Maycon Tavares Emílio Silva , Sérgio Alexandre Alcântara dos Santos , José Ricardo de Arruda Miranda , Clélia Akiko Hiruma Lima , Luis Antonio Justulin","doi":"10.1016/j.yexcr.2025.114464","DOIUrl":"10.1016/j.yexcr.2025.114464","url":null,"abstract":"<div><div>The developmental origins of health and disease (DOHaD) concept suggests that adverse conditions during gestation can influence the development and function of multiple organs, including the gastrointestinal tract. Maternal protein restriction (MPR) exposure has been associated with negative effects on reproduction, the endocrine system, and liver metabolic health. However, limited research has explored the impact of MPR on the offspring's intestinal morphophysiology. This study investigated the effects of gestational and lactational MPR on the duodenum and colon of young male offspring rats at postnatal (PND)21. We hypothesize that MPR affects intestinal morphophysiology and development early in life. Our findings revealed tachygastria in offspring exposed to MPR. The ultrastructural analysis uncovered a reduction in goblet cell numbers and changes in collagen deposition in the duodenum and colon. We also identified imbalances in inflammatory markers (IL-6 and TGF-β1) and antioxidant enzymes (CAT and SOD). These results demonstrate that MPR significantly affects gastrointestinal morphophysiology early in life by disrupting gastric motility and altering duodenal and colonic histoarchitecture, antioxidant defense, and inflammatory pathways. Such alterations may predispose the descendants to long-term gastrointestinal disorders, underscoring the importance of further research on the developmental origins of intestinal health and disease.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114464"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143471263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HOXD8 Drives Glioma Progression through Epithelial-Mesenchymal Transition Regulation: Implications for Prognosis and Targeted Therapy.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-18 DOI: 10.1016/j.yexcr.2025.114476

Ke Yu, Jiawei Meng, Tiange Chen, Yanshi Wang, Yi Zhao, Tianxiang Huang, Ge Gao

{"title":"HOXD8 Drives Glioma Progression through Epithelial-Mesenchymal Transition Regulation: Implications for Prognosis and Targeted Therapy.","authors":"Ke Yu, Jiawei Meng, Tiange Chen, Yanshi Wang, Yi Zhao, Tianxiang Huang, Ge Gao","doi":"10.1016/j.yexcr.2025.114476","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114476","url":null,"abstract":"<p><p>Glioma is one of the most common primary malignant tumors of the central nervous system. Here, we defined Homeobox D8 (HOXD8) as a novel biomarker for glioma utilizing RNA-sequencing and bioinformatics approaches. HOXD8 expression was significantly upregulated in glioma cell lines (U251 and U373) and clinical specimens compared to normal controls. Functional studies demonstrated that HOXD8 knockdown markedly inhibited glioma cell proliferation, migration, and invasion in vitro. Additionally, pan-cancer analysis revealed significant associations between HOXD8 expression and key tumor characteristics, including immune cell infiltratio, tumor mutational burde, and microsatellite instability. Meanwhile, transcriptomic profiling and pathway analysis identified HOXD8's involvement in epithelial-mesenchymal transition (EMT) regulation, with western blot validation showing significant modulation of EMT markers following HOXD8 knockdown. Collectively, our results suggests that HOXD8 may serve as a satisfactory prognostic biomarker that promotes glioma cell proliferation, migration and invasion,potentially through regulation of EMT processes.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114476"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A genome-wide CRISPR-Cas9 knockout screen using dynamin knockout cells identifies Nf2 and Traf3 as genes involved in dynamin-independent endocytosis.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-18 DOI: 10.1016/j.yexcr.2025.114470

Sho Takahashi, Mizuho Maehara, Chihiro Nishihara, Hiroyuki Iwata, Shusaku Shibutani

{"title":"A genome-wide CRISPR-Cas9 knockout screen using dynamin knockout cells identifies Nf2 and Traf3 as genes involved in dynamin-independent endocytosis.","authors":"Sho Takahashi, Mizuho Maehara, Chihiro Nishihara, Hiroyuki Iwata, Shusaku Shibutani","doi":"10.1016/j.yexcr.2025.114470","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114470","url":null,"abstract":"<p><p>Endocytosis is a fundamental process by which cells take up extracellular materials, including nutrients, growth factors, and pathogens. Although several endocytic pathways, such as clathrin-mediated and caveolin-mediated endocytosis, are well-characterized, other endocytic pathways remain poorly understood. Therefore, in this study, we performed a genome-wide CRISPR-Cas9 screen to elucidate new endocytic pathways using dynamin conditional knockout cells. We identified genes that significantly reduced the cell numbers when knocked out simultaneously with dynamin. Among these, neurofibromin 2 (Nf2) and tumor necrosis factor receptor-associated factor 3 (Traf3), whose relationship with endocytosis was not well understood, were investigated for their roles in endocytosis activity. Nf2 and Traf3 knockout cells exhibited reduced non-specific fluid endocytosis in a dynamin-independent manner. However, Nf2 or Traf3 knockout did not affect the transferrin receptor-mediated endocytosis that depends on clathrin and dynamin. Moreover, Nf2 knockout cells showed reduced cholera toxin uptake in a dynamin-independent manner. Overall, this study highlights the roles of Nf2 and Traf3 in endocytosis.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114470"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TRIM22 inhibits the metastasis of colorectal cancer through facilitating β-Catenin degradation

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-18 DOI: 10.1016/j.yexcr.2025.114473

Haiyang Hu, Wensheng Li, Pengfei Ma, Junxin Song, Xiaobo Zhang, Longhui Ruan, Jing Zhang, Youwei Zheng

{"title":"TRIM22 inhibits the metastasis of colorectal cancer through facilitating β-Catenin degradation","authors":"Haiyang Hu, Wensheng Li, Pengfei Ma, Junxin Song, Xiaobo Zhang, Longhui Ruan, Jing Zhang, Youwei Zheng","doi":"10.1016/j.yexcr.2025.114473","DOIUrl":"10.1016/j.yexcr.2025.114473","url":null,"abstract":"<div><div>Tripartite motif-containing 22 (TRIM22), a member of the tripartite motif protein family, has emerged as a putative tumor suppressor in various cancers. Nevertheless, its specific role and clinical significance in colorectal cancer (CRC) remain poorly characterized. Herein, we observed that TRIM22 expression was frequently downregulated in primary CRC tissues and was significantly correlated with better prognosis. Functional assays demonstrated that TRIM22 overexpression substantially attenuated the metastatic potential of CRC cells both in vitro and in vivo. Mechanistically, our results revealed that TRIM22 directly interacts with and ubiquitinates β-Catenin, a crucial transcription factor that drives CRC metastasis by modulating the epithelial-mesenchymal transition (EMT) process. Additionally, our data indicated that the anti-metastatic effect of TRIM22 relies on the degradation of β-catenin. In summary, this study is the first to deliberate the vital anti-tumor role of TRIM22 in CRC metastasis. We also provide new evidence suggesting that TRIM22 could be a prognostic marker and therapeutic target for inhibiting CRC progression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114473"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0