Regular ArticleConstitutive Expression of Human Ribosomal Protein L7 Arrests the Cell Cycle in G1and Induces Apoptosis in Jurkat T-Lymphoma Cells
Abstract
Protein L7 is involved in translational control in eucaryotic cells as indicated by its association with ribosomes, its capability to inhibit specifically the cell-free translation of distinct mRNAs, and its interference with the synthesis of two major nucleus-associated proteins in L7 cDNA-transfected Jurkat T-lymphoma cells [F. Neumannet al.(1995)Nucleic Acids Res.23, 195]. In this report we show that the constitutive expression of protein L7 in Jurkat cells leads to an arrest in G1of the cell cycle and induces apoptosis as a consequence of cell-to-cell contact. Treatment of the L7 transfectants with the inhibitor of translation cycloheximide, at doses which do not affect untransfected cells, enhances their sensitivity to the induction of apoptosis. These results suggest that L7 can interfere with the translation of proteins which control cell cycle progression and/or the initiation of the apoptotic pathway.
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Classifying Rheumatoid Arthritis gene network signatures for identifying key regulatory molecules and their altered pathways by adopting network biology approach
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RNA interference-mediated knockdown of SIRT1 and/or SIRT2 in melanoma: Identification of downstream targets by large-scale proteomics analysis
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Melanoma is the deadliest form of skin cancer, due to its aggressive nature, metastatic potential, and a lack of sufficient treatment options for advanced disease. Therefore, detailed investigations into the molecular mechanisms of melanoma growth and progression are needed. In the search for candidate genes to serve as therapeutic targets, the sirtuins show promise as they have been found to be upregulated in melanoma and they regulate a large number of proteins involved in cellular processes known to affect tumor growth, such as DNA damage repair, cell cycle arrest, and apoptosis. In this study, we used a large-scale label-free comparative proteomics system to identify novel protein targets that are affected following knockdown of SIRT1 and/or 2 in A375 metastatic melanoma cell line. Our study offers important insight into the potential downstream targets of SIRTs 1 and/or 2. This may unravel new potential areas of exploration in melanoma research.
Proteomic analysis of ovarian cancer cells during epithelial-mesenchymal transition (EMT) induced by epidermal growth factor (EGF) reveals mechanisms of cell cycle control
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Cancer is a complex multistep process characterized by accumulation of several hallmarks including epithelial to mesenchymal transition (EMT), which promotes cellular and microenvironmental changes resulting in invasion and migration to distant sites, favoring metastasis. EMT can be triggered by different extracellular stimuli, including growth factors such as EGF. In ovarian cancer, the most lethal gynecological cancer, overexpression of the EGFR family is associated with more aggressive clinical behavior, increasing mortality rate caused by metastasis. Our proteomic data, together with specific validation of specific cellular mechanisms demonstrated that EGF-induced EMT in Caov-3 cells leads to important alterations in metabolic process (protein synthesis) and cell cycle control, supporting the implication of EGF/EMT in cancer metastasis, cancer stem cell generation and, therefore, poor prognosis for the disease.
Identification of interacting partners of Human Mpv17-like protein with a mitigating effect of mitochondrial dysfunction through mtDNA damage
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