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Cell–Cell Communications through Gap Junctions and Cancer in 3D Systems
Published in Karen J.L. Burg, Didier Dréau, Timothy Burg, Engineering 3D Tissue Test Systems, 2017
Stephanie Nicole Shishido, Thu Annelise Nguyen
Metastasis is a complex process involving cellular dissociation, tissue invasion, transport of metastatic cells via blood or lymph, extravasation to a distant site, and formation of a secondary tumor. Loss of GJIC has been observed in metastatic disease (Nicolson et al. 1988; Behrens et al. 1989; Klaunig et al. 1990; Ren et al. 1990; Yamasaki 1990; Birchmeier et al. 1991). There are two steps in which gap junctions play a role in metastasis: (1) cellular dissociation and invasion and (2) extravasation at the secondary site. Evidence indicates that a loss of GJIC correlates with metastatic potential of the primary tumor. In a metastatic breast cancer cell line, transfection with the breast metastasis suppressor 1 (BRMS1) complementary DNA (cDNA) restores GJIC by increasing Cx43 expression and reducing Cx32, resulting in a more normal phenotype (Saunders et al. 2001). E-cadherin expression also correlates positively with GJIC (Mege et al. 1988; Jongen et al. 1991). A reduction in E-cadherin indicates a loss of co-operation between neighboring cells and reduced GJIC, leading to cellular dissociation in invasive tumors.
Illuminating the cycle of life
Published in Raquel Seruca, Jasjit S. Suri, João M. Sanches, Fluorescence Imaging and Biological Quantification, 2017
Anabela Ferro, Patrícia Carneiro, Maria Sofia Fernandes, Tânia Mestre, Ivan Sahumbaiev, João M. Sanches, Raquel Seruca
Our group focuses in understanding the role of adhesion molecules in cancer. A specific interest is the impact of a pivotal adhesion molecule in epithelia (E-cadherin) and its mediated signaling underlying cancer. In hereditary diffuse gastric cancer E-cadherin, mutations are causative events and in contrast to many other cancer type these carcinomas to do not show a high proliferation rate [128]. However, little is known concerning how E-cadherin alterations lead to cell-cycle deregulation or how the dynamics of cell cycle impact on E-cadherin expression and function. We recently found that eukaryotic cells expressing mutant E-cadherin moieties comprising a juxtamembrane mutation show varying protein expression profiles along the cell-cycle phases in contrast to wild-type E-cadherin expressing cells (Ferro et al., unpublished data). The distinctive E-cadherin expression profile observed in E-cadherin mutant cells in G1/G0 versus G2 phase may be possibly related to the activation of ERAD as a compensatory cellular mechanism. Although preliminary, these results open a new possibility of identifying molecular cofactors that can interfere with the profile of expression and function of mutant proteins, namely dysfunctional E-cadherin in cancer. Therapeutically, their identification is crucial to target such factors and circumvent the expression of unfolded proteins through the exploitation of cell-cycle proteins acting in G1/G0 phase. Interestingly, the growth suppressor properties of normal E-cadherin, in many carcinoma cells, are due to an increase in the expression and activity levels of p27Kip1 that lead to cell–cell contact inhibition and quiescence, with cell-cycle arrest at G1 phase [129]. In addition, p21Cip1 and p27Kip1 CDK inhibitors, which control G1/S phase transition, are often downregulated in gastric cancer (GC) [130].
Introduction to Cancer
Published in Anjana Pandey, Saumya Srivastava, Recent Advances in Cancer Diagnostics and Therapy, 2022
Anjana Pandey, Saumya Srivastava
The major alteration was found in the level of E-cadherin in different studies. Loss of E-cadherin function was found in the majority of cancer cells by inactivation of E-cadherin genes, repression of transcription, or inactivation by proteolysis of the extracellular domain.
Methanolic extract of Teucrium persicum up-regulates and induces the membrane restoration of E-cadherin protein in PC-3 cells
Published in International Journal of Environmental Health Research, 2023
Majid Tafrihi, Anahita Naeimi, Fatemeh Eizadifard
Over the last decades, the role of cadherins in tumor development has extensively been studied. Several studies have shown that the E-cadherin protein is a specific marker for epithelial tissues that regulates the occurrence of EMT (epithelial-mesenchymal transition). EMT that is identified by loss of cell adhesion, down-regulation of epithelial markers including E-cadherin and up-regulation of mesenchymal markers including N-cadherin, Vimentin, and Fibronectin, plays a pivotal role in embryonic development and tumorigenesis and promotes the metastasis of advanced tumors (Bruner and Derksen 2018). There is a body of evidence that the E-cadherin protein acts as a tumor suppressor and its functional disorders result in neoplastic growth and cancer (Cepowicz et al. 2017; Na et al. 2020).
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.
Polyclonal antibody production against rGPC3 and their application in diagnosis of hepatocellular carcinoma
Published in Preparative Biochemistry and Biotechnology, 2018
Shenghao Wang, Muhammad Kalim, Keying Liang, Jinbiao Zhan
One important aspect of invasion in HCC development is the transformation between epithelial and interstitial cells (EMT) that was considered to be an essential step in the process of metastasis.[11] In all the features of EMT, E-cadherin inhibition is one of the important markers. E-cadherin inhibition will lead primary cancer cells to leave its initial location, degraded in the extracellular matrix, migrated into blood vessels, and invade other organs finally.[12] Qi et al. reported that expression of GPC3 and E-cadherin is negatively correlated in HepG2 cells.[13] In addition, it was found that high expression of E-cadherin in primary hepatocellular carcinoma is also correlated with elevated expression of the GPC3 protein. Furthermore, EMT-like changes in GPC3-expressing HepG2 are more than those in Hep3B and Huh7, and the ability to metastasize is stronger than them. Some studies have also shown that GPC3 can induce tumor cell EMT-like changes to promote HCC cell metastasis and ERK signaling pathway that also involves GPC3-mediated invasion.[14] Ruan et al. also demonstrated that GPC3 is correlated with the migration of HCC cell in vitro and in vivo experiments.[15] These findings show that overexpression of GPC3 protein promotes EMT in HCC and tumor cell migration. It was reported that novel therapeutics development must be considered against GPC3 molecular target.[16]