China
Africa
Explore chapters and articles related to this topic
Chemopreventive Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Interestingly, the SNAIL signaling pathway triggers breast cancer metastasis but has no relevance in pancreatic cancer models. Also, EMT can be reversed via Mesenchymal-Epithelial Transition (MET) which is thought to facilitate the implanting of circulating tumor cells to develop secondary tumors when they reach a desirable target metastatic site. As part of this processes, the Extracellular Matrix (ECM) must be degraded, which is carried out by a proteolytic enzyme family, the Matrix Metalloproteinases (MMPs). These enzymes are key to tumor invasion, allowing tumor cells to degrade the ECM, penetrate the basement membrane, and move to other sites. MMPs also regulate cellular adhesion, which makes it easier for tumor cells to migrate. Cell Adhesion Molecules (CAMs) also play a significant role in tumor development and metastases, and include four groups: the Cadherins, Selectins, Integrins, and the Immunoglobulin Superfamily. A reduction or loss in Cadherin expression has been observed in some epithelial cancers, which is associated with increased invasion and metastasis. Activation of CAM proteins, including kinases and chemokines, can induce downstream signaling pathways, which ultimately promotes tumor growth and progression. Some chemopreventive agents are thought to work by inhibiting key regulators to suppress tumor invasion and metastasis.
Biological basis of angiogenesis and role of vascular endothelial growth factor-D
Published in A. R. Genazzani, Hormone Replacement Therapy and Cancer, 2020
The neovascularization and/or formation of lymphatic vessels in solid tumors is induced by tumor cells that express inductive angiogenic factors which promote vessels sprouting with the recruitment of endothelial cells to the growing tumor mass8,43,44. However, tumor vasculature is highly disorganized with vessels dilated, tortuous and fenestrated, with excessive branching and uneven diameters45. This could be the result of the imbalance of angiogenic factors. The fine regulation of VEGF-D by Cadherin signaling is probably compromised in tumor cells, especially considering that Cadherin expression is altered during the malignant progression of tumors46–51.
Host Defense I: Non-specific Immunity
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
The cadherin family of adhesion molecules are critical for the development of many tissues. These are calcium-dependent homophilic molecules which are very important in tissue structure, since their cytoplasmic domains anchor the cytoskeleton to the point of adhesion. These molecules are expressed early in development. In fact, uvomorulin is present on resting oocytes, and its synthesis increases at the two cell stage of the embryo. These molecules have not been ascribed specific immune recognition or regulatory function.
Suspended cell lines for inactivated virus vaccine production
Published in Expert Review of Vaccines, 2023
Jiayou Zhang, Zhenyu Qiu, Siya Wang, Zhenbin Liu, Ziling Qiao, Jiamin Wang, Kai Duan, Xuanxuan Nian, Zhongren Ma, Xiaoming Yang
The calcium dependent cell adhesins (cadherin) family is one of the earliest adhesion molecules that Takeichi discovered to mediate cell aggregation. In the presence of Ca2+, it can resist protease hydrolysis. The connection between the cytoskeleton transmembrane protein E-cadherin (also known as uvomorulin, L-CAM, cell CAM 120/80, or ARC-1) and actin filament is the key to cell-cell adhesion. Cells lacking E-cadherin expression do not aggregate or adhere to each other because the production of cadherin-catenin adhesion complexes is affected [106]. α-Catenin is a key subunit of the cadherin catenin adhesion complex, which affects cell-cell adhesion. In the absence of stable α-Catenin expression in poorly differentiated cell lines, the addition of α- Catenin cDNA will increase Ca2+-dependent cell-cell aggregation, indicating that α-Catenin directly leads to the loss of cell-cell adhesion in some cell lines [109]. In α-Catenin-ablated keratinocytes, cell-cell connection defects could be observed using immunofluorescence microscopy along with excessive cell proliferation [110].
Circ_0075804 Regulates the Expression of LASP1 by Targeting miR-1287-5p and Thus Affects the Biological Process of Retinoblastoma
Published in Current Eye Research, 2022
Qichao Han, Lan Ma, Li Shao, Hong Wang, Meiyan Feng
In view of the overexpression of circ_0075804 in RB cells, we knocked down circ_0075804 expression in SO-RB50 and Y79 cells to exploit the circ_0075804 function. As displayed in Figure 2A, circ_0075804 expression was remarkably reduced in these two cell lines containing sh-circ_0075804. Then, downregulation of circ_0075804 impaired cell viability reduced the number of EdU-positive cells and inhibited the number of colonies in SO-RB50 and Y79 cells, by CCK-8 (42% decrease in SO-RB50 cells and 55% decrease in Y79 cells), EdU (36% decrease in SO-RB50 cells and 44% decrease in Y79 cells) and colony formation (44% decrease in SO-RB50 cells and 50% decrease in Y79 cells) assays (Figure 2B–D), evidencing that cell proliferative capacity was suppressed by circ_0075804 knockdown. In contrast, by flow cytometry assay, downregulation of circ_0075804 increased the apoptosis rate of SO-RB50 and Y79 cells (Figure 2E). Transwell assay exhibited that SO-RB50 and Y79 cells with circ_0075804 downregulation had inhibitory invasive capacity (Figure 2F). As verification, we examined the expression of E-cadherin and N-cadherin. E-cadherin expression was heightened (64% increase in SO-RB50 cells and 86% increase in Y79 cells), while N-cadherin expression was lessened (39% decrease in SO-RB50 cells and 46% decrease in Y79 cells) in SO-RB50 and Y79 cells after circ_0075804 downregulation (Figure 2G,H), verifying the inhibition of cell invasion caused by circ_0075804 downregulation.
Altered expression of junctional proteins as a potential biomarker in oral precancerous and cancerous patients
Published in Tissue Barriers, 2022
Puja Upadhaya, Sarbani Giri, Dharmeswar Barhoi, Abhinandan Bhattacharjee
Cadherins are major components of AJs and serve a key role in the maintenance of epithelial tissue integrity.13 E-cadherin (E-cad) is a 120 KD transmembrane glycoprotein belonging to AJs and a major calcium-dependent cell surface adhesion molecule.14 It is encoded by the CDH1 gene located on chromosome 16q-224 and is restricted to the surface of the epithelial cells.15 It is a widely distributed, intercellular adhesion molecule16 that through its cytoplasmic tail, associates with various intracellular proteins.17 It functions in cellular crosstalk and mediates cell-to-cell communication by protein interactions on the cytoplasmic membrane surfaces. Reports suggest the role of E-cad as a biomarker in detecting gene expression and predicting disease progression.18 Therefore, investigation of E-cad might be a promising area of interest and could be a potential biological marker.