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Nuclear Factor Kappa-B: Bridging Inflammation and Cancer
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Mohammad Aslam Khan, Girijesh Kumar Patel, Haseeb Zubair, Nikhil Tyagi, Shafquat Azim, Seema Singh, Aamir Ahmad, Ajay Pratap Singh
NF-κB has been shown to control proliferation of normal as well as tumor cells by binding to the promoter of genes responsible for cell proliferation. Study published by Brantley and colleagues stated that NF-κB induces proliferation of mammary epithelial cells, suggesting the involvement of NF-κB in the development of mammary glands [90]. In triple negative breast cancer cells, NF-κB has been shown to exhibit trans-activity as it binds upstream of CD44 promoter and induces tumor cell proliferation [91]. Transformed cells grow continuously, circumventing cell cycle check, and NF-κB signaling indirectly controls cancer cell cycle progression by upregulating the expression of cyclin D, a regulator of G1 checkpoint control [92]. Furthermore, it has been shown that Rac1, a small GTPase, induces lung cancer cell proliferation, possibly through NF-κB activation [93].
Entamoeba histolytica
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Jesús Serrano-Luna, Moisés Martínez-Castillo, Nidia Leon-Sicairos, Mineko Shibayama, Mireya de la Garza
The complex relationship between host cells, gut microbiota, pathogenic bacteria, and E. histolytica is governed by inherent signaling systems, which play important roles in the infection progress30; for example, they have direct implications for parasite migration, proliferation, differentiation, locomotion, and metabolism.6,31 Many aspects of amoeba signaling have been found to be regulated by Ca2+, and diverse calcium proteins have been found in E. histolytica. The EhCaBP1 and EhCaBP3 are involved in actin bundling, which regulates parasite adhesion, phagocytosis, and proliferation,32–35 while URE3-BP and calmodulin have a direct effect in its virulence.36,37 The rearrangement of the actin cytoskeleton that participates in adhesion, motility, tissue invasion, and phagocytosis has been found to be regulated by heterotrimeric G-proteins. The role of Rab proteins has been widely studied in terms of intracellular signaling; these proteins are part of the Rho and Rac families.38–41
Identification of Novel ras Family Genes in A Human Teratocarcinoma Cell Line by Oligonucleotide Screening
Published in Juan Carlos Lacal, Frank McCormick, The ras Superfamily of GTPases, 2017
George T. Drivas, Mark G. Rush, Peter D’Eustachio
No additional functional studies have been done with the rho subfamily members TC25/rac 1 and TC10. Characterization of rac 1 and studies pertaining to the functions of rho group proteins can be found elsewhere in this volume.
The role of small GTPase Rac1 in ionizing radiation-induced testicular damage
Published in International Journal of Radiation Biology, 2022
Yasar Aysun Manisaligil, Mukaddes Gumustekin, Serap Cilaker Micili, Cemre Ural, Zahide Cavdar, Gizem Sisman, Aysegul Yurt
Small GTPases are involved in various physiological and pathological events such as cell growth, cytoskeleton reconstruction, protein kinase activation, ROS generation and regulation of endothelial permeability. In addition to two cytosolic proteins (p47phox, p67phox) small GTPase Rac1 is also required for the activation of NADPH oxidase in phagocytic cells (Takai et al. 2001). Furthermore, Rac1 has other cell cycle roles, cell adhesion, actin-dependent motility, and epithelial differentiation. The expression and/or activity of Rac1 has been shown to increase under pathological conditions such as oxidative stress and apoptosis (Boehm et al. 1999; Pervaiz et al. 2001). It is thought that Rac1 may play a role in radiation-induced damage considering its role in the generation of ROS and, as a subunit of the NADPH oxidase enzyme, its contribution in the generation of free radicals. In this study, we aimed to investigate the role of small GTPase Rac1 molecule in acute and late effects of low, medium and high dose radiation exposures (administered during diagnosis and/or treatment) on the testicular tissue.
EHD2 Overexpression Suppresses the Proliferation, Migration, and Invasion in Human Colon Cancer
Published in Cancer Investigation, 2021
Chengqi Guan, Cuihua Lu, Mingbing Xiao, Weichang Chen
It has been reported that EHD2 has interacted with EHBP1, which is an important molecule involved in actin microfilament assembly, and regulated cytoskeleton and polarity to promote malignant progression of tumors (12). EHD2 also regulates actin recombination to promote endocytosis by controlling Rac1 activity in tumorigenesis. Rac1 is involved in regulating the maintenance of cell polarity and cell migration through the regulation of GTPase activity and cytoskeleton rearrangement. It is an important signal transduction and polarity regulator in cells (32). This regulation of activity may significantly affect the EMT, which is closely related to invasion and distant metastasis of tumor cells (33). In agreement with these studies, other studies have reported that EHD2 can inhibit tumorigenesis in both hepatocellular carcinoma and breast cancer through the modulation of E-cadherin, the critical marker of EMT (34,35). E-cadherin is a calcium-dependent cellular adhesion molecule, which plays a key role in epithelial cell behavior, cancer inhibition, and tissue formation (36). Our results are in agreement with the results of previous studies, and our findings also suggested that E-cadherin is upregulated in SW620 cells with EHD2 overexpression. These results indicate that the increased E-cadherin activity achieved through promoting EHD2 activity may be an effective approach to treat cancer. EHD2 may be considered an E-cadherin modulator in colon cancer; furthermore, EHD2-induced colon cancer suppression may be controlled via diverse mechanisms, and this can be the future research direction.
Knockdown of lncRNA LSINCT5 suppresses growth and metastasis of human glioma cells via up-regulating miR-451
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Rac1, a member of the Rho GTPase family, appears to be deregulated in both expression and activity in diverse tumour cells [33]. Some studies reported that Rac1 was up-regulated in glioma and down-regulating Rac1 could greatly inhibit glioma cell growth [34,35]. In this study, Rac1 was the target of miR-451 which exhibited anticancer effect through negatively regulating Rac1. Thus, Rac1 might be involved in the actions of LSINCT5 and miR-451 in glioma cells. It was reported that Rac1 functioned as a critical mediator of tumour angiogenesis and metastasis through mediating several signal pathways [36]. The PI3K/AKT, Wnt/β-catenin and NF-κB activities regulated by Rac1 were related to many cancer types [37–40]. Since these three signallings were closely related to glioma development [26–28], the effect of LSINCT5-miR-451-Rac1 axis on these pathways in GL15 cells was explored. We found that the pathways were inhibited by LSINCT5 silence, miR-451 overexpression and Rac1 silence. Thereby we speculated that LSINCT5-miR-451-Rac1 axis impacted glioma cells growth and metastasis possibly by indirect mediating PI3K/AKT, Wnt/β-catenin and NF-κB pathways.