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Cell Adhesion & Migration最新文献

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Dual implication of endothelial adhesion molecules in tumor progression and cancer immunity. 内皮粘附分子在肿瘤进展和癌症免疫中的双重作用。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-03-12 DOI: 10.1080/19336918.2025.2472308
Louis-Emmanuel Chriqui, Sabrina Cavin, Jean Yannis Perentes
{"title":"Dual implication of endothelial adhesion molecules in tumor progression and cancer immunity.","authors":"Louis-Emmanuel Chriqui, Sabrina Cavin, Jean Yannis Perentes","doi":"10.1080/19336918.2025.2472308","DOIUrl":"10.1080/19336918.2025.2472308","url":null,"abstract":"<p><p>Adhesion molecules are proteins expressed at the surface of various cell types. Their main contribution to immunity is to allow the infiltration of immune cells in an inflamed site. In cancer, adhesion molecules have been shown to promote tumor dissemination favoring the development of metastasis. While adhesion molecule inhibition approaches were unsuccessful for cancer control, their importance for the generation of an immune response alone or in combination with immunotherapies has gained interest over the past years. Currently, the balance of adhesion molecules for tumor promotion/inhibition is unclear. Here we review the role of selectins, intercellular adhesion molecules (ICAM) and vascular cell adhesion molecules (VCAM) from the perspective of the dual contribution of adhesion molecules in tumor progression and immunity.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2472308"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11913389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603512","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
Loss of CDS1 impairs the tumorigenic characteristics of nasopharyngeal carcinoma by modulating lipid metabolism. CDS1的缺失通过调节脂质代谢损害鼻咽癌的致瘤性特征。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-06-25 DOI: 10.1080/19336918.2025.2520629
Yifang Wang, Limei Li, Liudmila Matskova, Lixian Deng, Danping Li, Yi Huang, Haili Liang, Wen Wang, Ziyuan Liang, Jiaming Su, Weilin Zhao, Tingting Huang, Jiemei Chu, Zhe Zhang, Xue Xiao, Xiaoying Zhou
{"title":"Loss of CDS1 impairs the tumorigenic characteristics of nasopharyngeal carcinoma by modulating lipid metabolism.","authors":"Yifang Wang, Limei Li, Liudmila Matskova, Lixian Deng, Danping Li, Yi Huang, Haili Liang, Wen Wang, Ziyuan Liang, Jiaming Su, Weilin Zhao, Tingting Huang, Jiemei Chu, Zhe Zhang, Xue Xiao, Xiaoying Zhou","doi":"10.1080/19336918.2025.2520629","DOIUrl":"10.1080/19336918.2025.2520629","url":null,"abstract":"<p><p>The accumulation of lipid droplets (LDs) enhancing nasopharyngeal carcinoma (NPC) cell migration. We reveals that CDP-diacylglycerol synthase 1 (CDS1), an inhibitor of LDs formation, is significantly downregulated in NPC. Restoring CDS1 expression suppresses NPC cell growth, colony formation, tumorigenesis, migration, and invasion. The anti-cancer effect of CDS1 is attributed to its role in decreasing the intracellular LDs. Moreover, CDS1 promotes activation of the NF-κB signaling pathway, resulting in elevated levels of inflammatory cytokines within NPC cells. This is likely to enhance the immunogenicity of these cells, thereby reducing tumor volume in the in vivo model. These findings establish CDS1 as a novel suppressor of NPC by modulating LDs levels, suggesting potential therapeutic avenues aimed at limiting LDs accumulation.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2520629"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494752","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
Pathological significance and therapeutic prospects of HCCS expression patterns in lung adenocarcinoma. 肺腺癌中HCCS表达模式的病理意义及治疗前景。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-07-04 DOI: 10.1080/19336918.2025.2520632
Pengfei Luo, Sixuan Wu, Zhimin Li, Shuangfeng Tan, Lijun Zeng, Yuanbing Tang, Lunqi Luo, Yuehua Li, Zhaohui Tang
{"title":"Pathological significance and therapeutic prospects of <i>HCCS</i> expression patterns in lung adenocarcinoma.","authors":"Pengfei Luo, Sixuan Wu, Zhimin Li, Shuangfeng Tan, Lijun Zeng, Yuanbing Tang, Lunqi Luo, Yuehua Li, Zhaohui Tang","doi":"10.1080/19336918.2025.2520632","DOIUrl":"10.1080/19336918.2025.2520632","url":null,"abstract":"<p><p>This study examines Holocytochrome c synthase (<i>HCCS</i>) expression in lung adenocarcinoma (LUAD) and its impact on the tumor immune environment. By analyzing multiple tumor databases, the research highlights <i>HCCS</i> expression patterns across various cancer types, focusing on its correlation with M2-type macrophages, which aid tumor progression. Findings show that high <i>HCCS</i> expressionin LUAD is associated with increased M2-type macrophages, and variations in <i>HCCS</i> levels influence immune cell infiltration and cancer therapy responsiveness. It suggests that <i>HCCS</i> significantly shapes the immune landscape within tumors, promoting growth and spread, and underscores its potential as a therapeutic target in LUAD and other cancers with similar expression profiles.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2520632"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12233882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559309","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
Orosomucoid 1 interacts with S100A12 and activates ERK signalling to expedite the advancement of bladder cancer. Orosomucoid 1与S100A12相互作用，激活ERK信号，加速膀胱癌的进展。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2024-12-07 DOI: 10.1080/19336918.2024.2434209
Zhe Liu, Xiaofeng Pu
{"title":"Orosomucoid 1 interacts with S100A12 and activates ERK signalling to expedite the advancement of bladder cancer.","authors":"Zhe Liu, Xiaofeng Pu","doi":"10.1080/19336918.2024.2434209","DOIUrl":"10.1080/19336918.2024.2434209","url":null,"abstract":"<p><p>The research endeavors to expound the role of ORM1 in bladder cancer (BCa) and the implied response mechanism. RT-qPCR and Western blotting examined ORM1 and S100A12 expression. Functional experiments assessed the cellular phenotypes. HDOCK and Co-IP confirmed the interaction of ORM1 and S100A12. Western blotting tested apoptosis- and ERK signaling-associated proteins. ORM1 and S100A12 were abundant in the BCa cells. ORM1 or S100A12 loss impaired cell proliferation, migration, and invasion, and aggravated cell apoptosis. ORM1 interacted with S100A12. ORM1 knockdown down-regulated S100A12 expression and inactivated ERK signaling.S100A12 overexpression or ERK activator reversed the impacts of ORM1 interference on ERK signaling and BCa cells. ORM1 mightdrive BCa via binding to S100A12 and activating ERK signaling.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"1-11"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11633163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791169","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
Telomerase inhibitors - TMPyP4, BIBR 1532 and imetelstat - alter the adhesion potential of breast cancer MCF7 and MDA-MB-231 cells that leads to impaired ability to form spheroids. 端粒酶抑制剂- TMPyP4， BIBR 1532和imetelstat -改变乳腺癌MCF7和MDA-MB-231细胞的粘附潜力，导致形成球状体的能力受损。
IF 3.5 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-10-13 DOI: 10.1080/19336918.2025.2571328
Przemysław Kopczyński, Aleksandra Romaniuk-Drapała, Kinga Rygiel, Jacek Kujawski, Błażej Rubiś
{"title":"Telomerase inhibitors - TMPyP4, BIBR 1532 and imetelstat - alter the adhesion potential of breast cancer MCF7 and MDA-MB-231 cells that leads to impaired ability to form spheroids.","authors":"Przemysław Kopczyński, Aleksandra Romaniuk-Drapała, Kinga Rygiel, Jacek Kujawski, Błażej Rubiś","doi":"10.1080/19336918.2025.2571328","DOIUrl":"https://doi.org/10.1080/19336918.2025.2571328","url":null,"abstract":"<p><p>We assessed the influence of telomerase inhibitors TMPyP4, BIBR 1532, or imetelstat on the ability of MCF7 and MDA-MB-231 breast cancer cells to form spheroids. TMPyP4 significantly impaired the adhesion potential and ability of both cell lines to form spheroids. BIBR 1532 treatment did not show any effect in MCF7 while it showed some effect in MDA-MB-231 cells, although this effect was less extensive comparing to TMPyP4. Application of Imetelstat provoked a dispersion effect in both cell lines but more single, separated distant cells were observed. Molecular docking and molecular dynamic studies showed that both BIBR 1532 and TMPyP4 exhibited affinity toward the structure of a G-quadruplex of human telomeric RNA (TERRA2 G4s) and the catalytic subunit of telomerase, hTERT. We showed that the use of telomerase expression/activity inhibitors to reduce the adhesive capacity and metastatic potential of breast cancer cells may play a significant role in anticancer strategy.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2571328"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285783","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
Fe3O4 nanoparticles containing gambogic acid inhibit metastasis in colorectal cancer via the RORB/EMILIN1 axis. 含有甘草酸的Fe3O4纳米粒子通过RORB/EMILIN1轴抑制结直肠癌转移
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-12-01 Epub Date: 2024-11-13 DOI: 10.1080/19336918.2024.2427585
Xiaodong Fan, Chunyang Lv, Meiling Xue, Peng Meng, Xiaoping Qian
{"title":"Fe<sub>3</sub>O<sub>4</sub> nanoparticles containing gambogic acid inhibit metastasis in colorectal cancer via the RORB/EMILIN1 axis.","authors":"Xiaodong Fan, Chunyang Lv, Meiling Xue, Peng Meng, Xiaoping Qian","doi":"10.1080/19336918.2024.2427585","DOIUrl":"10.1080/19336918.2024.2427585","url":null,"abstract":"<p><p>This research aims to study the effect of magnetic nanoparticles of Fe3O4 (MNP Fe3O4) containing gambogic acid (GA-MNP Fe3O4) on colorectal cancer (CRC). MNP Fe3O4 enhanced the antitumor effect of GA by inhibiting the malignant behavior of CRC cells. RORB was a target of GA, and GA activated RORB expression to inhibit metastasis of CRC. Knockdown of RORB impaired the effect of GA-MNP Fe3O4 on CRC metastasis. EMILIN1 was a target of RORB, and RORB promoted transcription of EMILIN1. Overexpression of EMILIN1 reversed the effect of knockdown of RORB on GA-MNP Fe3O4 and inhibited metastasis in CRC. These findings revealed that MNP Fe3O4 enhanced the antitumor effect of GA and activated RORB to promote EMILIN1 transcription and inhibit CRC metastasis.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"18 1","pages":"38-53"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11562916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614407","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
Knockdown of PIK3R6 impedes the onset and advancement of clear cell renal cell carcinoma. 敲除 PIK3R6 会阻碍透明细胞肾细胞癌的发生和发展。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-12-01 Epub Date: 2024-06-03 DOI: 10.1080/19336918.2024.2353920
Jia Yang, Xiaoni Zhong, Xiaoling Gao, Wenyi Xie, Yaokai Chen, Yuanjiang Liao, Peilin Zhang
{"title":"Knockdown of PIK3R6 impedes the onset and advancement of clear cell renal cell carcinoma.","authors":"Jia Yang, Xiaoni Zhong, Xiaoling Gao, Wenyi Xie, Yaokai Chen, Yuanjiang Liao, Peilin Zhang","doi":"10.1080/19336918.2024.2353920","DOIUrl":"10.1080/19336918.2024.2353920","url":null,"abstract":"<p><p>In this research, we investigated the role of PIK3R6, a regulatory subunit of PI3Kγ, known for its tumor-promoting properties, in clear cell renal cell carcinoma (CCRCC). Utilizing the UALCAN website, we found PIK3R6 upregulated in CCRCC, correlating with lower survival rates. We compared PIK3R6 expression in CCRCC tumor tissues and adjacent normal tissues using immunohistochemistry. Post RNA interference-induced knockdown of PIK3R6 in 786-O and ACHN cell lines, we performed CCK-8, colony formation, Edu staining, flow cytometry, wound healing, and transwell assays. Results showed that PIK3R6 silencing reduced cell proliferation, migration, and invasion, and induced G0/G1 phase arrest and apoptosis. Molecular analysis revealed decreased CDK4, Cyclin D1, N-cadherin, Vimentin, Bcl-2, p-PI3K and p-AKT, with increased cleaved caspase-3, Bax, and E-cadherin levels in CCRCC cells. Moreover, inhibiting PIK3R6 hindered tumor growth. These findings suggest a significant role for PIK3R6 in CCRCC cell proliferation and metastasis, presenting it as a potential therapeutic target.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"18 1","pages":"1-12"},"PeriodicalIF":3.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11152098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141236410","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
JNK3 inhibitors as promising pharmaceuticals with neuroprotective properties. JNK3 抑制剂是一种具有神经保护特性的有前途的药物。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-12-01 Epub Date: 2024-02-15 DOI: 10.1080/19336918.2024.2316576
Yibeini Wu, Yiling Zhao, Ziman Guan, Sajjad Esmaeili, Zhicheng Xiao, Diji Kuriakose
{"title":"JNK3 inhibitors as promising pharmaceuticals with neuroprotective properties.","authors":"Yibeini Wu, Yiling Zhao, Ziman Guan, Sajjad Esmaeili, Zhicheng Xiao, Diji Kuriakose","doi":"10.1080/19336918.2024.2316576","DOIUrl":"10.1080/19336918.2024.2316576","url":null,"abstract":"<p><p>The intensive study and investigation of neuroprotective therapy for central nervous system (CNS) diseases is ongoing. Due to shared mechanisms of neurodegeneration, a neuroprotective approach might offer benefits across multiple neurological disorders, despite variations in symptoms or injuries. C-Jun N-terminal Kinase 3 (JNK3) is found primarily in the CNS and is involved in physiological processes such as brain development, synapse formation, and memory formation. The potential of JNK3 as a target for pharmacological development holds promise for advancing neuroprotective therapies. Developing small molecule JNK3 inhibitors into drugs with neuroprotective qualities could facilitate neuronal restoration and self-repair. This review focuses on elucidating key neuroprotective mechanisms, exploring the interplay between neurodegenerative diseases and neuroprotection, and discussing advancements in JNK3 inhibitor drug development.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"18 1","pages":"1-11"},"PeriodicalIF":3.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10878020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139734604","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
The relationship between endoplasmic reticulum stress and apoptosis in the process of adipose-derived stromal cells differentiating into astrocytes. 脂肪基质细胞分化为星形胶质细胞过程中内质网应激与细胞凋亡之间的关系
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-12-01 Epub Date: 2024-11-19 DOI: 10.1080/19336918.2024.2430561
Pingshu Zhang, Wen Li, Ya Ou, Qi Yan, Qi Wu, Xiaodong Yuan
{"title":"The relationship between endoplasmic reticulum stress and apoptosis in the process of adipose-derived stromal cells differentiating into astrocytes.","authors":"Pingshu Zhang, Wen Li, Ya Ou, Qi Yan, Qi Wu, Xiaodong Yuan","doi":"10.1080/19336918.2024.2430561","DOIUrl":"10.1080/19336918.2024.2430561","url":null,"abstract":"<p><p>The potential of adult adipose-derived stromal cells (ADSCs) to differentiate into astrocytes holds promise for future cell transplantation therapies. However, the growth of differentiated astrocytes is unstable, and their survival rate is low. Endoplasmic reticulum (ER) pathway mediated apoptosis is one of the causes of cell death, but whether there is ER stress response in the differentiation of ADSCs into astrocytes is still unclear. In this study, the expression of protein factors related to endoplasmic reticulum stress (ERS) and apoptosis, including GRP78, ATF6, PERK, CHOP, Caspase12, and Caspase3, was detected in cells. It was found that the expression of ERS pro-survival factors was highest in the ADSCs group and decreased with prolonged induction time. Conversely, the expression levels of pro-apoptotic factors increased with the extension of induction time. Thus, ERS occurs during the differentiation of ADSCs into astrocytes, and ERS can mediate apoptosis of ADSC-derived astrocytes.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"18 1","pages":"54-65"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11581194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675272","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
Cell adhesion and migration in disease: translational and therapeutic opportunities. 疾病中的细胞粘附和迁移：转化和治疗机会。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-12-01 Epub Date: 2024-06-11 DOI: 10.1080/19336918.2024.2362978
Kurt Anderson, Yolanda Calle-Patino, Aleksandar Ivetic, Maddy Parsons, Ferran Valderrama, Claire Wells, Ines Anton
{"title":"Cell adhesion and migration in disease: translational and therapeutic opportunities.","authors":"Kurt Anderson, Yolanda Calle-Patino, Aleksandar Ivetic, Maddy Parsons, Ferran Valderrama, Claire Wells, Ines Anton","doi":"10.1080/19336918.2024.2362978","DOIUrl":"10.1080/19336918.2024.2362978","url":null,"abstract":"<p><p>In September 2023 members of the cell adhesion and cell migration research community came together to share their latest research and consider how our work might be translated for clinical practice. Alongside invited speakers, selected speakers and poster presentations, the meeting also included a round table discussion of how we might overcome the challenges associated with research translation. This meeting report seeks to highlight the key outcomes of that discussion and spark interest in the cell adhesions and cell migration research community to cross the perceived valley of death and translate our work into therapeutic benefit.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"18 1","pages":"1-3"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11174059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300093","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
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