Background: The ribosomal protein S6 kinase 1 (S6K1) is one of the main components of the mTOR/S6K signal transduction pathway, which controls cellular metabolism, autophagy, growth, and proliferation. Overexpression of S6K1 was detected in tumors of different origin including breast cancer, and correlated with the worse disease outcome. In addition, significant accumulation of S6K1 was found in the nuclei of breast carcinoma cells suggesting the implication of kinase nuclear substrates in tumor progression. However, this aspect of S6K1 functioning is still poorly understood. The main aim of the present work was to study the subcellular localization of S6K1 in breast cancer cells with the focus on cell migration. Methods: Multicellular spheroids of MCF-7 cells were generated using agarose-coated Petri dishes. Cell migration was induced by spheroids seeding onto adhesive growth surface and subsequent cultivation for 24 to 72 hours. The subcellular localization of S6K1 was studied in human normal breast and cancer tissue samples, 2D and 3D MCF-7 cell cultures using immunofluorescence analysis and confocal microscopy. Results: Analysis of histological sections of human breast tissue samples revealed predominantly nuclear localization of S6K1 in breast malignant cells and its mainly cytoplasmic localization in conditionally normal cells. In vitro studies of MCF-7 cells demonstrated that the subcellular localization of S6K1 depends on the cell density in the monolayer culture. S6K1 relocalization from the cytoplasm into the nucleus was detected in MCF-7 cells migrating from multicellular spheroids onto growth surface. Immunofluorescence analysis of S6K1 and immunocoprecipitation assay revealed the colocalization and interaction between S6K1 and transcription factor TBR2 (T-box brain protein 2) in MCF-7 cells. Conclusions: Subcellular localization of S6K1 depends on the density and locomotor activity of the MCF-7 cells.
Aim.We intend to characterize the new peptide-specific antibodies against the isoform 2 of translation elongation factor 1A (eEF1A2) and determine its presence in the postoperative samples of human breast, lung and stomach tumor tissues. Methods. The analysis of antibody specificity was performed by enzyme-linked immunosorbent assay, immunoblotting and immunohistochemistry. Immunoblotting and immunohistochemistry were used for the determination of the eEF1A2 in the human tumor samples, as well as in the samples of normal tissues surrounding tumors. Results. The antibodies obtained against the eEF1A2 specifically recognized this protein in the cell extracts and histological sections and did not cross-react with the elongation factor 1A isoform 1. eEF1A2 was revealed in the postoperative samples of breast, lung and stomach tumors as well as in the putative normal tissues surrounding tumors. Conclusions. The antibodies obtained against eEF1A2 are highly specific for the antigen and can be used for the immunological studies of tumors.
We compare the effects of an extremely low-frequency electromagnetic field (EMF) with the chemotherapeutic agent doxorubicin (DOX) on tumor growth and the hepatic redox state in Walker-256 carcinosarcoma-bearing rats. Animals were divided into five groups with one control (no tumor) and four tumor-bearing groups: no treatment, DOX, DOX combined with EMF and EMF. While DOX and DOX + EMF provided greater inhibition of tumor growth, treatment with EMF alone resulted in some level of antitumor effect (p < .05). Superoxide dismutase, catalase activity and glutathione content were significantly decreased in the liver of tumor-bearing animals as compared with the control group (p < .05). The decreases in antioxidant defenses accompanied histological findings of suspected liver damage. However, hepatic levels of thiobarbituric acid reactive substances, an indicator of lipid peroxidation, were three times lower in EMF and DOX + EMF groups than in no treatment and DOX (p < .05). EMF and DOX + EMF showed significantly lower activity of serum ALT than DOX alone (p < .05). These results indicate that EMF treatment can inhibit tumor growth, causing less pronounced oxidative stress damage to the liver. Therefore, EMF can be used as a therapeutic strategy to influence the hepatic redox state and combat cancer with reduced sideeffects.
The aim is to reveal the immunohistochemical features of human papilloma virus type 16 expression in various histological variants of pleomorphic adenomas of the salivary gland. Materials and methods: The material of the study was surgical and biopsy material from 30 patients with pleomorphic adenomas of the salivary glands, among which in 15 cases mesenchymal was detected, in 10 – mixed, in 5 cases – epithelial histological variant, respectively. Immunohistochemical study was performed, using mouse monoclonal antibody to human papilloma virus type 16. Visualization was performed, using an EnVisionTM FLEX detection system. Histological sections of grade III cervical intraepithelial neoplasia (CIN III) were used as a positive control; for a negative control, the procedure was performed without primary antibodies. The immunohistochemical reaction was assessed by a semi-quantitative method by counting the percentage of positively stained cells in the field of view of a microscope × 400. Microspecimens were studied, photoarchived on an Olympus BX-41 microscope. Results: Expression of human papilloma virus type 16 of varying severity was determined in 26 cases of pleomorphic adenomas of the salivary glands, which was 86.7%. The epithelial component of the pleomorphic adenoma of the salivary gland was characterized by a more pronounced expression of the monoclonal antibody to human papilloma virus type 16 compared to the mesenchymal component of the tumor. The severity of the immunohistochemical reaction with a monoclonal antibody to human papilloma virus type 16 depended on the histological variant of the pleomorphic adenoma of the salivary gland. Epithelial, mixed and mesenchymal variants of pleomorphic adenoma of the salivary gland were characterized, respectively, by the most pronounced, pronounced and moderately pronounced expression of a monoclonal antibody to human papilloma virus type 16. Conclusions: A comprehensive immunohistochemical study with a monoclonal antibody to human papilloma virus type 16 revealed the presence of a causal relationship between the infection of a patient with human papilloma virus type 16 and development of pleomorphic adenoma of the salivary gland in him.
The ribosomal protein S6 kinase 1 (S6K1) is one of the main Background: components of the mTOR/S6K signal transduction pathway, which controls cellular metabolism, autophagy, growth, and proliferation. Overexpression of S6K1 was detected in tumors of different origin including breast cancer, which was associated with a worse disease outcome. In addition, significant accumulation of S6K1 was found in the nuclei of breast carcinoma cells suggesting the implication of kinase nuclear substrates in tumor progression. However, this aspect of S6K1 functioning is poorly understood. The main aim of the present work was to study the subcellular localization of S6K1 in breast cancer cells with focus on cell migration.Multicellular spheroids of MCF-7 cells were generated using Methods: agarose-coated Petri dishes. Cell migration was initiated by spheroids seeding onto growth surface and subsequent cultivation for 24 and 72 hours. S6K1 subcellular localization was studied in human breast cancer and normal tissue, 2D and 3D MCF-7 cell culture using immunofluorescence analysis and confocal microscopy.Analysis of histological sections of human breast cancer and Results: normal tissue revealed predominantly nuclear localization of S6K1 in breast malignant cells and mainly cytoplasmic one in conditionally normal cells. In studies of MCF-7 cells showed that the subcellular localization of S6K1 vitro depends on the cell density in the monolayer culture. S6K1 relocalization from the cytoplasm into the nucleus was detected in MCF-7 cells migrating from multicellular spheroids onto growth surface. Immunofluorescence analysis of S6K1 and immunocoprecipitation assay revealed the colocalization and interaction between S6K1 and transcription factor TBR2 (T-box brain protein 2) in MCF-7 cells. Bioinformatical analysis revealed existence of several phosphorylation sites in TBR2 for S6K1 suggesting that TBR2 can be a target for phosphorylation and regulation by S6K1. 2018, 7:1332 Last updated: 17 MAY 2019 that TBR2 can be a target for phosphorylation and regulation by S6K1.Subcellular localization of S6K1 depends on the density and Conclusions: locomotor activity of the MCF-7 cells.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.