Effect of Dexmedetomidine-Mediated Insulin–LikeGrowthFactor2 (IGF2) Signal Pathway on Immune Function and Invasion and Migration of Cancer Cells in Rats with Ovarian Cancer.
by Kayla
No Comments
BACKGROUND The purpose of this study was to explore the effects of dexmedetomidine (DEX) -mediated insulin-like growth factor 2 (IGF2) signaling pathway in immune functions and cancer cell invasion and migration in mice with ovarian cancer. MATERIALS AND METHODS Forty mice with ovarian cancer were divided into 4 groups: the model group and low dose (0.2 mg / kg / h DEX), medium dose (1.0 ug / kg / h DEX), and high dose ( 5.0 mg / kg / h DEX) DEX group. In addition, 10 Fischer344 rats selected as normal group.
Human NUTU 19 poorly differentiated epithelial ovarian cancer cells were divided into 4 groups: empty and low-dose, medium-dose and high-dose DEX NUTU-19 group. RESULTS Compared with normal group, other groups serum interleukin (IL) -2 and interferon gamma (INF-γ) levels, CD4⁺ and CD8⁺ percentages, ratios CD4⁺ / CD8⁺, and spleen lymphocyte transformation rate decreases, and the alpha serum tumor necrosis factor (TNF-alpha) levels, IGF2, insulin-like growth factor 1 receptor (IGF1R), insulin receptor substrate 1 (IRS1) mRNA and protein expression in ovarian tissue increased (all P <0.05).
Results in the DEX group compared with the model group are the opposite of those in the control group compared with the normal group (all P <0.05). Compared with blank group, other groups proliferation, invasion, and migration of ovarian cancer cells reduced significantly (all P <0.05). Compared with low doses of DEX NUTU-19 groups, in high doses of DEX-19 group NUTU invasion and migration of ovarian cancer cells weakened significantly (both P <0.05).
Conclusion A certain dose DEX can effectively inhibit the activation of signaling pathways IGF2 to enhance the immune function of mice with ovarian cancer, inhibits invasion and migration of ovarian cancer cells.
Effect of Dexmedetomidine-Mediated Insulin–LikeGrowthFactor2 (IGF2) Signal Pathway on Immune Function and Invasion and Migration of Cancer Cells in Rats with Ovarian Cancer.
Insulin-like growth factor II mRNA binding protein 3 promotes cell proliferation, migration and invasion in human glioblastoma.
Background / Purpose: Recently, insulin-like growth factor-binding protein mRNA 3 (IMP3) has been reported to be involved in tumorigenesis. We aim to study the expression and role of IMP3 in human glioblastoma. Methods: We analyzed the expression of IMP3 in 70 cases of glioma tissue, normal brain tissue and 5 of cell lines using western blot. Immunohistochemistry (IHC) was used to evaluate the expression and distribution of IMP3 in glioma tissue. colony formation, wound healing, migration and invasion tests and tumorigenesis in nude mice were used to explore the IMP3 function in vitro and in vivo.
The epithelial-mesenchymal transition (EMT) -related biomarkers detected by Western blot. Results: We found that the expression levels of IMP3 was significantly higher in glioma tissue than that in normal brain tissue and glioma associated with the class. In-vitro tests revealed that excessive IMP3 was significantly induced cell proliferation, migration, and invasion. Mechanically, IMP3 over-expression downregulated the expression of E-cadherin, but upregulated the expression of N-cadherin, vimentin, snails, slugs and MMP9.
However, inhibition of oncogenic effects IMP3 disorders. In vivo assay also showed that silencing of IMP3 inhibit tumor growth and increased survival of tumor-bearing nude mice xenograft. Conclusion: IMP3 can promote cell proliferation, migration and invasion by inducing EMT in glioblastoma. Thus, targeting the pathway IMP3 may be a new way to treat patients with glioblastoma.Schizophrenia associated with abnormal neural development of the brain, the IGF-2 (insulin-like growth factor-2) had a major impact.
Description: Western blot, 0.1-0.5μg/ml, Human, Mouse, Rat;_x000D_Immunohistochemistry (Paraffin-embedded Section), 0.5-1μg/ml, Human, Rat, Mouse, By Heat;_x000D_Immunocytochemistry/Immunofluorescence, 5 μg/ml, Human
Description: A Monoclonal antibody against Human IGF1R / IGF1 Receptor. The antibodies are raised in Mouse. This antibody is applicable in WB and IHC-P, E, Flo
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human IGF1R / IGF1 Receptor (aa1126-1175). This antibody is tested and proven to work in the following applications:
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human IGF1 Receptor (IGF1R) (N-term). This antibody is tested and proven to work in the following applications:
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human IGF1 Receptor (IGF1R) (C-term). This antibody is tested and proven to work in the following applications:
Description: Boster Bio IGF1R mouse monoclonal antibody, clone OTI4C4 (formerly 4C4). Catalog# M00070-1. Tested in FC, WB. This antibody reacts with Human, Mouse, Rat.
Description: A Monoclonal antibody against Human IGF1R / IGF1 Receptor (clone 1H7). The antibodies are raised in Mouse and are from clone 1H7. This antibody is applicable in WB and IHC-P, Flo
Description: A Monoclonal antibody against Human IGF1R / IGF1 Receptor (aa1264-1367, clone JBW902). The antibodies are raised in Mouse and are from clone JBW902. This antibody is applicable in WB and IHC-P, IP
Description: IGF-I receptor is a disulfide-linked heterotetrameric transmembrane protein consisting of two alpha and two beta subunits. Both the alpha and beta subunits are encoded within a single receptor precursor cDNA. The proreceptor polypeptide is proteolytically cleaved and disulfide-linked to yield the mature heterotetrameric receptor. The alpha subunit of IGF-I receptor is extracellular while the beta subunit has an extracellular domain, a transmembrane domain and a cytoplasmic tyrosine kinase domain. The IGF-I receptor is highly expressed in all cell types and tissues.
Description: Available in various conjugation types.
×
The purpose of this study was to evaluate serum levels and IGF-2 binding protein IGFBP-3 and IGFBP-7 in patients with schizophrenia and the association of this protein with schizophrenia psychopathology and cognitive deficits
