Relevant bibliographies by topics / Mesenchymal-amoeboid transition (MAT)

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Mesenchymal-amoeboid transition (MAT)'

Author: Grafiati
Published: 14 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Mesenchymal-amoeboid transition (MAT)"

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Merta, Ladislav, Aneta Gandalovičová, Vladimír Čermák, et al. "Increased Level of Long Non-Coding RNA MALAT1 Is a Common Feature of Amoeboid Invasion." Cancers 12, no. 5 (2020): 1136. http://dx.doi.org/10.3390/cancers12051136.

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The ability of cancer cells to adopt various migration modes (the plasticity of cancer cell invasiveness) is a substantive obstacle in the treatment of metastasis, yet still an incompletely understood process. We performed a comparison of publicly available transcriptomic datasets from various cell types undergoing a switch between the mesenchymal and amoeboid migration modes. Strikingly, lncRNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) was one of three genes that were found upregulated in all amoeboid cells analyzed. Accordingly, downregulation of MALAT1 in predominantly
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Taylor, Sophie, Sabine Knipp, Arndt Rohwedder, et al. "ANGI-03. THE MIGRATORY SWITCH – INVESTIGATING MESENCHYMAL-AMOEBOID TRANSITION (MAT) IN HIGH GRADE GLIOMAS." Neuro-Oncology 19, suppl_6 (2017): vi22. http://dx.doi.org/10.1093/neuonc/nox168.082.

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Ketchen, Sophie E., Filomena O. Gamboa-Esteves, Sean E. Lawler, et al. "Drug Resistance in Glioma Cells Induced by a Mesenchymal–Amoeboid Migratory Switch." Biomedicines 10, no. 1 (2021): 9. http://dx.doi.org/10.3390/biomedicines10010009.

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Cancer cell invasion is a precondition for tumour metastasis and represents one of the most devastating characteristics of cancer. The development of drugs targeting cell migration, known as migrastatics, may improve the treatment of highly invasive tumours such as glioblastoma (GBM). In this study, investigations into the role of the cell adhesion protein Cellular communication network factor 1 (CCN1, also known as CYR61) in GBM cell migration uncovered a drug resistance mechanism adopted by cells when treated with the small molecule inhibitor CCG-1423. This inhibitor binds to importin α/β in
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Liu, Yixin, Ya-Jun Wang, Yang Du, et al. "DNA nanomachines reveal an adaptive energy mode in confinement-induced amoeboid migration powered by polarized mitochondrial distribution." Proceedings of the National Academy of Sciences 121, no. 14 (2024). http://dx.doi.org/10.1073/pnas.2317492121.

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Energy metabolism is highly interdependent with adaptive cell migration in vivo. Mechanical confinement is a critical physical cue that induces switchable migration modes of the mesenchymal-to-amoeboid transition (MAT). However, the energy states in distinct migration modes, especially amoeboid-like stable bleb (A2) movement, remain unclear. In this report, we developed multivalent DNA framework-based nanomachines to explore strategical mitochondrial trafficking and differential ATP levels during cell migration in mechanically heterogeneous microenvironments. Through single-particle tracking a
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Rodríguez-Cruz, Daniela, Aleix Boquet-Pujadas, Eunice López-Muñoz, et al. "Three-dimensional cell culture conditions promoted the Mesenchymal-Amoeboid Transition in the Triple-Negative Breast Cancer cell line MDA-MB-231." Frontiers in Cell and Developmental Biology 12 (August 2, 2024). http://dx.doi.org/10.3389/fcell.2024.1435708.

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IntroductionBreast cancer (BC) is the leading cause of death among women, primarily due to its potential for metastasis. As BC progresses, the extracellular matrix (ECM) produces more type-I collagen, resulting in increased stiffness. This alteration influences cellular behaviors such as migration, invasion, and metastasis. Specifically, cancer cells undergo changes in gene expression that initially promote an epithelial-to-mesenchymal transition (EMT) and subsequently, a transition from a mesenchymal to an amoeboid (MAT) migration mode. In this way, cancer cells can migrate more easily throug
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Sachdeva, Ashwin, Claire A. Hart, Kyungmin Kim, et al. "Non-canonical EphA2 activation underpins PTEN-mediated metastatic migration and poor clinical outcome in prostate cancer." British Journal of Cancer, July 22, 2022. http://dx.doi.org/10.1038/s41416-022-01914-3.

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Abstract Background The key process of mesenchymal to amoeboid transition (MAT), which enables prostate cancer (PCa) transendothelial migration and subsequent development of metastases in red bone marrow stroma, is driven by phosphorylation of EphA2S897 by pAkt, which is induced by the omega-6 polyunsaturated fatty acid arachidonic acid. Here we investigate the influence of EphA2 signalling in PCa progression and long-term survival. Methods The mechanisms underpinning metastatic biopotential of altered EphA2 signalling in relation to PTEN status were assessed in vitro using canonical (EphA2D73
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Ross, Emily C., Arne L. ten Hoeve, and Antonio Barragan. "Integrin-dependent migratory switches regulate the translocation of Toxoplasma-infected dendritic cells across brain endothelial monolayers." Cellular and Molecular Life Sciences, May 22, 2021. http://dx.doi.org/10.1007/s00018-021-03858-y.

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AbstractMultiple cellular processes, such as immune responses and cancer cell metastasis, crucially depend on interconvertible migration modes. However, knowledge is scarce on how infectious agents impact the processes of cell adhesion and migration at restrictive biological barriers. In extracellular matrix, dendritic cells (DCs) infected by the obligate intracellular protozoan Toxoplasma gondii undergo mesenchymal-to-amoeboid transition (MAT) for rapid integrin-independent migration. Here, in a cellular model of the blood–brain barrier, we report that parasitised DCs adhere to polarised endo
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Dissertations / Theses on the topic "Mesenchymal-amoeboid transition (MAT)"

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Leo, Angela. "The study of cell motility and plasticity in cancer: the role of the crosstalk between BM-MSCs and tumor in osteosarcoma progression and Claisened Hexafluoro as potential inhibitor of amoeboid motility in metastatic melanoma." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1128636.

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Part 1 Growing evidence suggest that bone marrow-derived mesenchymal stem cells (BM-MSCs) are key players in tumor stroma. Here, we investigated the cross-talk between BM-MSCs and osteosarcoma (OS) cells in tumor progression. We revealed a strong tropism of BM-MSCs towards these tumor cells and identified monocyte chemoattractant protein (MCP)-1, growth-regulated oncogene (GRO)-α and transforming growth factor (TGF)-β1 as pivotal factors for BM-MSC chemotaxis. Once in contact with OS cells, BM-MSCs trans-differentiate into cancer-associated fibroblasts, further increasing MCP-1, GRO-α, inter
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Cartier-Michaud, Amandine. "Etude de l'influence du PAI-1 matriciel sur la régulation de la transition Mésenchymo-Amiboïde des cellules cancéreuses." Phd thesis, Université d'Evry-Val d'Essonne, 2010. http://tel.archives-ouvertes.fr/tel-00875713.

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La transition cellulaire Mésenchymo-Amiboïde (MAT) est requise pour l'échappement métastasique, cependant elle n'a encore jamais été associée à une situation physiopathologique précise. PAI-1, l'inhibiteur de l'activateur du plasminogène de type-1, est une molécule du microenvironnement tumoral considérée comme facteur de mauvais pronostic et localisée en forte concentration autour des tumeurs les plus invasives. Nous montrons que, sous sa forme matricielle active, PAI-1 est capable d'entretenir, au cours du temps et de façon dose-dépendante, la morphologie amiboïde de cellules cancéreuses col
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