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CelIs as physical objects
Published in A. Šiber, P. Ziherl, Cellular Patterns, 2018
Cell‐cell adhesion is the fundamental physical process responsible for the existence of tissues. At the molecular scale, adhesion is caused by transmembrane proteins from the cadherin superfamily. There are hundreds of different cadherin types found in animals [27]. Cadherin molecules are anchored in the membrane (Figure 2.10), with their intracellular component attached to contractile actin‐filament bundles of the cell cortex. Their extra‐cellular part binds to a cadherin on the surface of the neighboring cell [28]. Regions of membrane where cells bind to each other are called adherens junctions. In epithelia, they are arranged in a belt‐like formation known as the adhesion belt running around the cell circumference.
Biomechanics of Cancer
Published in Adil Al-Mayah, Biomechanics of Soft Tissues, 2018
Homeyra Pourmohammadali, Mohammad Kohandel, Sivabal Sivaloganathan
The ability of cells to bind with other normal and cancerous cells or to the surrounding ECM changes during carcinogenesis. This ability can change depending on the stage of cancer progression and on the cell phenotype (Katira et al., 2013). One of the important transmembrane proteins that has a functional role in cell adhesion is cadherin. The increasing malignancy results in more P-cadherin binding between cells (Van Marck et al., 2005) and less E-cadherin-mediated adhesion (Bryan et al., 2008). Mathematical models have been used to study the effect of cell-adhesion changes, in particular the relationship between internal pressure of the tumor and surface tension, which is a function of cell–cell adhesion (Byrne and Chaplain, 1996).
in situ fluorescence microscopic images of cancer cell populations
Published in Raquel Seruca, Jasjit S. Suri, João M. Sanches, Fluorescence Imaging and Biological Quantification, 2017
Joana Figueiredo, Ana Sofia Ribeiro, Tânia Mestre, Sofia Esménio, Martina Fonseca, Joana Paredes, Raquel Seruca, João M. Sanches
In cancer, E-cadherin deregulation is a common event, resulting, in most of the cases, in its absence or decreased expression at the cell membrane, as well as in aberrant expression at the cytoplasm, causing loss of protein function [23,32,33]. Contrarily, P-cadherin upregulation is frequently found in many tumor types and it is an effective marker of invasive capacity of cancer cells, since it interferes with the normal function of E-cadherin [34–39]. Further, altered expression of β- and p120-catenins have been reported to be associated with E-cadherin loss/decreased expression or function and, thus, their expression delocalization have already been proposed as prognostic factors in some carcinomas [40].
Regulation of stem cell fate and function by using bioactive materials with nanoarchitectonics for regenerative medicine
Published in Science and Technology of Advanced Materials, 2022
Wei Hu, Jiaming Shi, Wenyan Lv, Xiaofang Jia, Katsuhiko Ariga
For commonly used covalently crosslinked hydrogels, the dynamic mechanical properties are often derived from cell-mediated degradation. Khetan et al. encapsulated human mesenchymal stem cells (hMSCs) in covalently crosslinked hyaluronic acid hydrogels subjected to a multi-step crosslinking protocol, from cell–mediated–degradable to non-degradable [126]. They demonstrate that the differentiation of hMSCs is directed by the generation of traction force mediated through cellular degradation of matrix. Furthermore, their work emphasizes the type of hydrogel underlying the mechanism by which stem cells respond to biophysical cues. Heilshorn et al. demonstrate that the maintenance of neural progenitor cell (NPC) stemness in 3D hydrogels is dependent on matrix degradability but interestingly is independent of cytoskeletal tension and integrin-binding ligand clustering [127]. According to their work, the underlying mechanism is increased cadherin-mediated cell–cell contact and activating β-catenin signalling. Moreover, they demonstrate that NPC proliferation and differentiation also require increased degradability. Following this study, they further clarify the role of matrix remodelling on NPC differentiation and maturation [128]. Permitting 7-day matrix remodelling prior to induction of differentiation, NPCs can differentiate into astrocytes or mature functional neurons. It is attributed to up-regulating YAP expression via cadherin-mediated cell–cell contact.
Atmospheric fine particulate matter and epithelial mesenchymal transition in pulmonary cells: state of the art and critical review of the in vitro studies
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Margaux Cochard, Frédéric Ledoux, Yann Landkocz
Mesenchymal markers were studied more comprehensively. An elevation in N-cadherin expression was correlated with drug resistance, more specifically EGFR tyrosine kinase inhibitors in NSCLC (Zhang et al. 2013), but drug resistance as a consequence of EMT was since challenged (Yang et al. 2020). Still, N-cadherin might serve as a possible biomarker for EMT. Cadherin 11, also called OB-cadherin, is aberrantly expressed in malignant cells which display an invasive and metastatic phenotype, leading to fibrosis (Agarwal 2014). Expression of vimentin, a widely studied biomarker, was significantly increased in 49% of NSCLC patients, associated with metastasis and a poor overall survival prognosis (Dauphin et al. 2013; Tadokoro et al. 2016). Ancel et al. (2019) examined a combination of vimentin and the inhibitory checkpoint marker PDL-1 to enable detection of the most advanced cases and worst outcomes in NSCLC. Surface markers such as integrins were reviewed and among these αVβ6, α3β1 and α5β1 which are overexpressed in NSCLC patients stand out as possible clinical biomarkers (Agarwal 2014; Aksorn and Chanvorachote 2019).
Gold nanoparticles induce G2/M cell cycle arrest and enhance the expression of E-cadherin in breast cancer cells
Published in Inorganic and Nano-Metal Chemistry, 2020
Shaimaa Abdel-Ghany, Mennatallah Mahfouz, Nada Ashraf, Hussein Sabit, Emre Cevik, Mokhtar El-Zawahri
E-cadherin, encoded by CDH1 gene, is a transmembrane glycoprotein that confer homotypic interactions on the surface of a neighboring cell, a transmembrane domain, and a cytoplasmic domain that binds to members of the catenin protein family to transduce signals to the cell.[20]CDH1 is downregulated in several types of cancers including BC.[21] Because is responsible for metastasis and progression of the disease, restoring its activity is a potential way to control BC.[22] It is not known whether AuNPs can affect CDH1, however, elucidating this association might help to design therapeutic strategies accordingly. On the other hand, targeting other genes that colocalize with familial types-related genes such as BRC2 is a potential way to regulate its action. Partner and localizer of BRCA2 (PALB2) is one of these genes that coexist with BRCA2 in the nucleus.[23]PALB2 was found to be upregulated in BC,[24] hence, treatments that inhibit its expression is useful. Similarly, the association between AuNPs and PALB2 expression was not highlighted. Therefore, the present study aimed at investigating the association between AuNPs exposure of BC cells and the expression profile of CDH1 and PALB2.