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α- Linolenic acid modulates phagocytosis and endosomal pathways of extracellular Tau in microglia. α-亚麻酸调节小胶质细胞吞噬和细胞外Tau蛋白的内体通路。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2021-12-01 DOI: 10.1080/19336918.2021.1898727
Smita Eknath Desale, Subashchandrabose Chinnathambi
{"title":"α- Linolenic acid modulates phagocytosis and endosomal pathways of extracellular Tau in microglia.","authors":"Smita Eknath Desale, Subashchandrabose Chinnathambi","doi":"10.1080/19336918.2021.1898727","DOIUrl":"10.1080/19336918.2021.1898727","url":null,"abstract":"<p><p>Microglia, the resident immune cells, were found to be activated to inflammatory phenotype in Alzheimer's disease (AD). The extracellular burden of amyloid-β plaques and Tau seed fabricate the activation of microglia. The seeding effect of extracellular Tau species is an emerging aspect to study about Tauopathies in AD. Tau seeds enhance the propagation of disease along with its contribution to microglia-mediated inflammation. The excessive neuroinflammation cumulatively hampers phagocytic function of microglia reducing the clearance of extracellular protein aggregates. Omega-3 fatty acids, especially docosahexaenoic acid and eicosapentaenoic acid, are recognized to induce anti-inflammatory phenotype of microglia. In addition to increased cytokine production, omega-3 fatty acids enhance phagocytic receptors expression in microglia. In this study, we have observed the phagocytosis of extracellular Tau in the presence of α-linolenic acid (ALA). The increased phagocytosis of extracellular Tau monomer and aggregates have been observed upon ALA exposure to microglia cells. After internalization, the degradation status of Tau has been studied with early and late endosomal markers Rab5 and Rab7. Further, the lysosome-mediated degradation of internalized Tau was studied with LAMP-2A, a lysosome marker. The enhanced migratory ability in the presence of ALA could be beneficial for microglia to access the target and clear it. The increased migration of microglia was found to induce the microtubule-organizing center repolarization. The data indicate that the dietary fatty acids ALA could significantly enhance phagocytosis and intracellular degradation of internalized Tau. Our results suggest that microglia could be influenced to reduce extracellular Tau seed with dietary fatty acids.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"15 1","pages":"84-100"},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2021.1898727","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25492209","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: 10
The roles of serotonin in cell adhesion and migration, and cytoskeletal remodeling. 血清素在细胞粘附和迁移以及细胞骨架重塑中的作用。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2021-12-01 DOI: 10.1080/19336918.2021.1963574
Joe Anand Kumar John Jayakumar, Mitradas M Panicker
{"title":"The roles of serotonin in cell adhesion and migration, and cytoskeletal remodeling.","authors":"Joe Anand Kumar John Jayakumar, Mitradas M Panicker","doi":"10.1080/19336918.2021.1963574","DOIUrl":"10.1080/19336918.2021.1963574","url":null,"abstract":"<p><p>Serotonin is well known as a neurotransmitter. Its roles in neuronal processes such as learning, memory or cognition are well established, and also in disorders such as depression, schizophrenia, bipolar disorder, and dementia. However, its effects on adhesion and cytoskeletal remodelling which are strongly affected by 5-HT receptors, are not as well studied with some exceptions for e.g. platelet aggregation. Neuronal function is strongly dependent on cell-cell contacts and adhesion-related processes. Therefore the role played by serotonin in psychiatric illness, as well as in the positive and negative effects of neuropsychiatric drugs through cell-related adhesion can be of great significance. In this review, we explore the role of serotonin in some of these aspects based on recent findings.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"15 1","pages":"261-271"},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8437456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39396843","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
Long noncoding RNA ENST00000508435 promotes migration of breast cancer via FXR 1. 长链非编码RNA ENST00000508435通过fxr1促进乳腺癌迁移
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2021-12-01 DOI: 10.1080/19336918.2021.1921402
Luying Li, Youping Jin, Xue Wang, Li Wang, Yangbai Sun, Yihong Luo, Xiaojian Ni, Qi Lu, Wenbo Wei, Xiuling Zhi, Jerry Yu, Wei Zhu, Ping Zhou
{"title":"Long noncoding RNA <i>ENST00000508435</i> promotes migration of breast cancer via FXR 1.","authors":"Luying Li,&nbsp;Youping Jin,&nbsp;Xue Wang,&nbsp;Li Wang,&nbsp;Yangbai Sun,&nbsp;Yihong Luo,&nbsp;Xiaojian Ni,&nbsp;Qi Lu,&nbsp;Wenbo Wei,&nbsp;Xiuling Zhi,&nbsp;Jerry Yu,&nbsp;Wei Zhu,&nbsp;Ping Zhou","doi":"10.1080/19336918.2021.1921402","DOIUrl":"https://doi.org/10.1080/19336918.2021.1921402","url":null,"abstract":"<p><p>LncRNA plays a critical role in tumor progression. However, the role it executes in breast cancer is still unclear. Here, we report a newly discovered lncRNA, <i>ENST00000508435</i>, which could be remarkably up-regulated in breast cancer cells and tissues. We found that the expression of <i>ENST00000508435</i> was positively correlated with tumor size, lymph node metastasis and HER2. More interesting, overexpression of <i>ENST00000508435</i> significantly increased cell migration, while specific knockdown led to the opposite. RNA pull-down and RNA immunoprecipitation assays demonstrated that <i>ENST00000508435</i> could directly bind to FXR1 to promote tumor metastasis. <i>ENST00000508435</i> and FXR1 were positively correlated. FXR1 was also significantly up-regulated in breast tumors. Taken together, we propose that <i>ENST00000508435</i> regulates FXR1 to promote breast cancer metastasis.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"15 1","pages":"140-151"},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2021.1921402","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38955206","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: 2
Keratin 19 maintains E-cadherin localization at the cell surface and stabilizes cell-cell adhesion of MCF7 cells. 角蛋白 19 可维持 E-cadherin 在细胞表面的定位，并稳定 MCF7 细胞的细胞间粘附性。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2021-12-01 DOI: 10.1080/19336918.2020.1868694
Sarah Alsharif, Pooja Sharma, Karina Bursch, Rachel Milliken, Van Lam, Arwa Fallatah, Thuc Phan, Meagan Collins, Priya Dohlman, Sarah Tiufekchiev, Georges Nehmetallah, Christopher B Raub, Byung Min Chung
{"title":"Keratin 19 maintains E-cadherin localization at the cell surface and stabilizes cell-cell adhesion of MCF7 cells.","authors":"Sarah Alsharif, Pooja Sharma, Karina Bursch, Rachel Milliken, Van Lam, Arwa Fallatah, Thuc Phan, Meagan Collins, Priya Dohlman, Sarah Tiufekchiev, Georges Nehmetallah, Christopher B Raub, Byung Min Chung","doi":"10.1080/19336918.2020.1868694","DOIUrl":"10.1080/19336918.2020.1868694","url":null,"abstract":"<p><p>A cytoskeletal protein keratin 19 (K19) is highly expressed in breast cancer but its effects on breast cancer cell mechanics are unclear. In MCF7 cells where K19 expression is ablated,<i>we found that K19 is required to maintain rounded epithelial-like shape and tight cell-cell adhesion. A loss of K19 also lowered cell surface E-cadherin levels. Inhibiting internalization restored cell-cell adhesion of <i>KRT19</i></i>  knockout cells, suggesting that E-cadherin internalization contributed to defective adhesion. Ultimately, while K19 inhibited cell migration and invasion, it was required for cells to form colonies in suspension. Our results suggest that K19 stabilizes E-cadherin complexes at the cell membrane to maintain cell-cell adhesion which inhibits cell invasiveness but provides growth and survival advantages for circulating tumor cells.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"15 1","pages":"1-17"},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7801129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38779085","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
Mast cell tryptase enhances wound healing by promoting migration in human bronchial epithelial cells. 肥大细胞胰蛋白酶通过促进人支气管上皮细胞的迁移来促进伤口愈合。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2021-12-01 DOI: 10.1080/19336918.2021.1950594
Sofia Mogren, Frida Berlin, Sangeetha Ramu, Asger Sverrild, Celeste Porsbjerg, Lena Uller, Cecilia K Andersson
{"title":"Mast cell tryptase enhances wound healing by promoting migration in human bronchial epithelial cells.","authors":"Sofia Mogren,&nbsp;Frida Berlin,&nbsp;Sangeetha Ramu,&nbsp;Asger Sverrild,&nbsp;Celeste Porsbjerg,&nbsp;Lena Uller,&nbsp;Cecilia K Andersson","doi":"10.1080/19336918.2021.1950594","DOIUrl":"https://doi.org/10.1080/19336918.2021.1950594","url":null,"abstract":"<p><p>Epithelial damage and increase of intraepithelial mast cells (MC) are characteristics of asthma. The role of MC mediator tryptase and the protease-activated receptor-2 (PAR2) on epithelial wound healing is not fully investigated. Stimulation of bronchial epithelial cells (BECs) with tryptase promoted gap closure, migration and cellular speed compared to controls. Stimulated BECs had higher expression of migration marker CD151 compared to controls. Proliferation marker KI67 was upregulated in tryptase-stimulated BECs compared to controls. Treatment with PAR2 antagonist I-191 reduced gap closure, migration and cell speed compared to BECs stimulated with tryptase. We found that tryptase enhances epithelial wound healing by increased migration and proliferation, which is in part regulated via PAR2. Our data suggest that tryptase might be beneficial in tissue repair under baseline conditions. However, in a pathological context such as asthma with increased numbers of activated MCs, it might lead to epithelial remodeling and loss of function.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"15 1","pages":"202-214"},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2021.1950594","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39221709","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: 8
Role of tight junction-associated MARVEL protein marvelD3 in migration and epithelial-mesenchymal transition of hepatocellular carcinoma. 紧密连接相关的MARVEL蛋白marvelD3在肝癌迁移和上皮间质转化中的作用。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2021-12-01 DOI: 10.1080/19336918.2021.1958441
Yanmeng Li, Teng Li, Donghu Zhou, Jia Wei, Zhenkun Li, Xiaojin Li, Siyu Jia, Qin Ouyang, Saiping Qi, Zhibin Chen, Bei Zhang, Jing Yu, Jidong Jia, Anjian Xu, Jian Huang
{"title":"Role of tight junction-associated MARVEL protein marvelD3 in migration and epithelial-mesenchymal transition of hepatocellular carcinoma.","authors":"Yanmeng Li,&nbsp;Teng Li,&nbsp;Donghu Zhou,&nbsp;Jia Wei,&nbsp;Zhenkun Li,&nbsp;Xiaojin Li,&nbsp;Siyu Jia,&nbsp;Qin Ouyang,&nbsp;Saiping Qi,&nbsp;Zhibin Chen,&nbsp;Bei Zhang,&nbsp;Jing Yu,&nbsp;Jidong Jia,&nbsp;Anjian Xu,&nbsp;Jian Huang","doi":"10.1080/19336918.2021.1958441","DOIUrl":"https://doi.org/10.1080/19336918.2021.1958441","url":null,"abstract":"<p><p>MarvelD3, a recently identified tight junction membrane protein, could be associated with hepatocellular carcinoma (HCC). We aimed to investigate the role of marvelD3 in Epithelial-Mesenchymal Transition (EMT) and migration of HCC and explore the underlying molecular mechanisms. First, we assessed marvlD3 expression in HCC and normal liver tissues and found loss of marvelD3 expression was significantly correlated with the occurrence and TNM stage of HCC. Second, we detected that marvelD3 was downregulated in HCC cells with transforming growth factor β1 and snail/slug-induced EMT. Finally, we analyzed expression of marvelD3 protein was significantly associated with EMT and the NF-κB signaling pathway. Our study demonstrated that MarvelD3 inhibited EMT and migration of HCC cells along with inhibiting NF-κB signaling pathway.<b>Abbreviations:</b><b>HCC</b>, Hepatocellular carcinoma; <b>TJ</b>, Tight junction; <b>MARVEL</b>, MAL and related proteins for vesicle trafficking and membrane link; <b>EMT</b>, Epithelial<b>-</b>mesenchymal transition; <b>NF-κB</b>, Nuclear factor kappa B; <b>TAMPs</b>, Tight junction-associated marvel proteins; <b>TGF-β1</b>, Transforming growth factor-β1; <b>MMP9</b>, matrix metallopeptidase 9; <b>RT-PCR</b>, Real-time PCR; <b>IHC</b>, Immunohistochemistry; <b>IF</b>, Immunofluorescence.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"15 1","pages":"249-260"},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8331009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39267843","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: 7
Creation and use of organoids in biomedical research and healthcare: the bioethical and metabioethical issues. 类器官在生物医学研究和保健中的创造和使用:生物伦理学和代谢伦理学问题。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2021-12-01 DOI: 10.1080/19336918.2021.1996749
Henri-Corto Stoeklé, Achille Ivasilevitch, Geneviève Marignac, Christian Hervé
{"title":"Creation and use of organoids in biomedical research and healthcare: the bioethical and metabioethical issues.","authors":"Henri-Corto Stoeklé,&nbsp;Achille Ivasilevitch,&nbsp;Geneviève Marignac,&nbsp;Christian Hervé","doi":"10.1080/19336918.2021.1996749","DOIUrl":"https://doi.org/10.1080/19336918.2021.1996749","url":null,"abstract":"<p><p>In the field of bioethics, scientific articles have already been published, and have highlighted relatively pluralist reflections concerning the creation and use of organoids. This plurality, rather than simply reflecting the complexity of the subject, may also be a consequence of the multiple theoretical and practical frameworks applied. Moreover, the creation and use of organoids in biomedical research and healthcare is probably in its infancy. This phenomenon is likely to increase in amplitude. Bioethics may be able to provide it with an effective and pertinent moral meaning, provided that a veritable metabioethical reflection is developed in parallel, that is, a reflection on bioethics itself, to provide scientists and clinicians with the best possible assistance in their everyday practice.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"15 1","pages":"285-294"},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8555554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39566397","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: 9
SLPI facilitates cell migration by regulating lamellipodia/ruffles and desmosomes, in which Galectin4 plays an important role. SLPI通过调节板足/褶边和桥粒来促进细胞迁移，其中galectin - 4起重要作用。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2020.1829264
Yusuke Mizutani, Daisuke Omagari, Manabu Hayatsu, Masaaki Nameta, Kazuo Komiyama, Yoshikazu Mikami, Tatsuo Ushiki
{"title":"SLPI facilitates cell migration by regulating lamellipodia/ruffles and desmosomes, in which Galectin4 plays an important role.","authors":"Yusuke Mizutani,&nbsp;Daisuke Omagari,&nbsp;Manabu Hayatsu,&nbsp;Masaaki Nameta,&nbsp;Kazuo Komiyama,&nbsp;Yoshikazu Mikami,&nbsp;Tatsuo Ushiki","doi":"10.1080/19336918.2020.1829264","DOIUrl":"https://doi.org/10.1080/19336918.2020.1829264","url":null,"abstract":"<p><p>To elucidate the underlying mechanism of secretory leukocyte protease inhibitor (SLPI)-induced cell migration, we compared SLPI-deleted human gingival carcinoma Ca9-22 (ΔSLPI) cells and original (wild-type: wt) Ca9-22 cells using several microscopic imaging methods and gene expression analysis. Our results indicated reduced migration of ΔSLPI cells compared to wtCa9-22 cells. The lamellipodia/dorsal ruffles were smaller and moved slower in ΔSLPI cells compared to wtCa9-22 cells. Furthermore, well-developed intermediate filament bundles were observed at the desmosome junction of ΔSLPI cells. In addition, <i>Galectin4</i> was strongly expressed in ΔSLPI cells, and its forced expression suppressed migration of wtCa9-22 cells. Taken together, SLPI facilitates cell migration by regulating lamellipodia/ruffles and desmosomes, in which Galectin4 plays an important role.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"195-203"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2020.1829264","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38453883","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: 3
The focal adhesion protein Integrin-Linked Kinase (ILK) as an important player in breast cancer pathogenesis. 局灶黏附蛋白整合素连接激酶(ILK)在乳腺癌发病机制中起重要作用。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2020.1829263
Katerina Tsirtsaki, Vasiliki Gkretsi
{"title":"The focal adhesion protein Integrin-Linked Kinase (ILK) as an important player in breast cancer pathogenesis.","authors":"Katerina Tsirtsaki,&nbsp;Vasiliki Gkretsi","doi":"10.1080/19336918.2020.1829263","DOIUrl":"https://doi.org/10.1080/19336918.2020.1829263","url":null,"abstract":"<p><p>Cell-extracellular matrix interactions, or focal adhesions (FA), are crucial for tissue homeostasis but are also implicated in cancer. Integrin-Linked Kinase (ILK) is an abundantly expressed FA protein involved in multiple signaling pathways. Here, we reviewed the current literature on the role of ILK in breast cancer (BC). Articles included in vitro and in vivo experiments as well as studies in human BC samples. ILK attenuation via silencing or pharmaceutical inhibition, leads to apoptosis or inhibition of epithelial-to-mesenchymal transition, and cell invasion whereas ILK overexpression suppresses anoikis and promotes tumor growth and metastasis. Finally, ILK is upregulated in BC tumors and its expression is associated with grade, and metastasis. Therefore, ILK should be evaluated as a potential anti-cancer pharmaceutical target.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"204-213"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2020.1829263","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38478130","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: 13
KLF5 regulates epithelial-mesenchymal transition of liver cancer cells in the context of p53 loss through miR-192 targeting of ZEB2. 在p53缺失的情况下，KLF5通过miR-192靶向ZEB2调控肝癌细胞的上皮-间质转化。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2020.1826216
Lan Sun, Xiaona Zhou, Yanmeng Li, Wei Chen, Shanna Wu, Bei Zhang, Jingyi Yao, Anjian Xu
{"title":"KLF5 regulates epithelial-mesenchymal transition of liver cancer cells in the context of p53 loss through miR-192 targeting of ZEB2.","authors":"Lan Sun,&nbsp;Xiaona Zhou,&nbsp;Yanmeng Li,&nbsp;Wei Chen,&nbsp;Shanna Wu,&nbsp;Bei Zhang,&nbsp;Jingyi Yao,&nbsp;Anjian Xu","doi":"10.1080/19336918.2020.1826216","DOIUrl":"https://doi.org/10.1080/19336918.2020.1826216","url":null,"abstract":"<p><p>Krüppel-like factor 5 (KLF5) can both promote and suppress cell migration, but the underlying mechanisms have not been elucidated. In this study, we show that the function of KLF5 in epithelial-mesenchymal transition (EMT) and migration of liver cancer cells depends on the status of the cellular tumor antigen p53 (p53). Furthermore, zinc finger E-box-binding homeobox 2 (ZEB2) is the main regulator of KLF5 in EMT in liver cancer cells in the context of p53 loss. Most importantly, the regulation of ZEB2 by p53 and KLF5 is indirect and that miR-192 mediates this regulation. Finally, we find that in invasive liver cancer, KLF5 is absent in the context of p53 loss or mutation.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"182-194"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2020.1826216","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38507019","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: 7
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