Regular ArticleConstitutive Expression of Human Ribosomal Protein L7 Arrests the Cell Cycle in G1and Induces Apoptosis in Jurkat T-Lymphoma Cells
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2018, Gene ReportsCitation Excerpt :So A2M can be potentially targeted to regulate and limit its action on VEGF to maintain the normal metabolism of the body. In patients with chronic systemic autoimmune disorders, RPL7 has been reported as an auto-antigen representing a significant target for autoantibodies and has been established that the expression of RPL7 inhibits cell cycle and promotes/induces apotopsis in T-lymphoma cells (Mikecz et al., 1995; Neumann and Krawinkel, 1997). As mentioned in sub-network studies SPP1, highly up-regulated non-essential gene, on further investigation revealed its influential role in the pathogenesis of RA.
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2018, Journal of ProteomicsCitation Excerpt :Increased expression of RPS5 in murine leukemia cells results in decreased levels of the cyclin-dependent kinases CDK2, CDK4, and CDK6, indicating an anti-proliferative role in these cells [36]. While RPL7 was shown to be overexpressed in some cancers, its constitutive expression in Jurkat T-lymphoma cells induces G1 cell cycle arrest and apoptosis [37]. Extra-ribosomal roles for RPS10 and RPL27 are not clearly defined, however, both are frequently mutated in Diamond-Blackfan anemia, a condition associated with a predisposition to several types of cancer [33].
Proteomic analysis of ovarian cancer cells during epithelial-mesenchymal transition (EMT) induced by epidermal growth factor (EGF) reveals mechanisms of cell cycle control
2017, Journal of ProteomicsCitation Excerpt :In addition to the role of ribosomal stabilization and maintenance of the efficiency and accuracy of translation, the RPs have also demonstrated secondary functions, or extra-ribosomal functions, related to other cellular processes including proliferation, cell cycle and gene expression [51–53]. Overexpression of RP L41 can arrest the cell cycle at the G1 phase in human lung carcinoma H1299 cells through an increase in p21Cip1/Waf1 levels, while constitutive overexpression of RP L7 in Jurkat T-lymphoma cells leads to G1 arrest via the modulation of cell cycle progression related proteins [54,55]. In our data, EGF-induced EMT was able to impair the transition from G1 to S phase by maintaining high levels of p21Cip1/Waf1, which block the G1/S transition, independent of p53 modulation (Fig. 5).
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