The Effects of the Transforming GrowthFactor-β1 (TGF-β1) Signaling Pathway on Cell Proliferation and Cell Migration are Mediated by Ubiquitin Specific Protease 4 (USP4) in Hypertrophic Scar Tissue and Primary Fibroblast Cultures.
Results BACKGROUND Hypertrophic scar from an abnormal repair response trauma to the skin and involves the proliferation of fibroblasts with collagen deposition increases. Transforming growth factor-ß1 (TGF-ß1) and TGF-ß receptor type I (TGF-SSR1) are involved in tissue repair and increased ubiquitin-specific protease 4 (USP4). This study aimed to investigate the effect of TGF-SSR1 and USP4 in human tissue samples hypertrophic scars and cell proliferation and cell migration in primary fibroblast cultures in vitro.
MATERIALS AND METHODS Skin excision of tissue samples with adjacent normal skin was obtained from 15 patients with hypertrophic scars, which provides part of the network and the primary fibroblast culture for analysis. Immunohistochemistry detected the expression of TGF-SSR1 USP4 and in parts of the network. MicroRNA (miRNAs) expression levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR).
Western blot performed to measure the level of protein expression. cultured skin fibroblasts was investigated using immunofluorescence staining. fibroblast proliferation, apoptosis, and migration was measured by Cell Counting Kit-8 (CCK-8) assay, flow cytometry, and the test wound healing, respectively.
RESULTS Expression USP4 and TGF-SSR1 in hypertrophic scar increased compared with normal skin. Cultured fibroblasts from hypertrophic scar tissue showed increased expression of TGF-USP4 and SSR1. Fibroblasts transfected with USP4 short interfering RNA (siRNA) resulted in a decrease fibroblast proliferation and migration, and increased apoptosis. Downregulation of USP4 inhibits the expression of TGF-SSR1 protein and increase levels of Smad7 protein expression. CONCLUSION USP4 regulated proliferation, migration, and apoptosis of hypertrophic scars fibroblasts with TGF-ß1 regulate signaling pathways.
The Effects of the Transforming GrowthFactor-β1 (TGF-β1) Signaling Pathway on Cell Proliferation and Cell Migration are Mediated by Ubiquitin Specific Protease 4 (USP4) in Hypertrophic Scar Tissue and Primary Fibroblast Cultures.
Role fibroblast growth factor 4 in growth and metastasis of colorectal cancer.
The role of fibroblast growth factor receptor 4 (FGFR4) in colorectal cancer (CRC) is poorly marked. Therefore, the purpose of this study was to determine the level of expression of FGFR4 in colorectal cancer and prognostic value, as well as clarify the role of FGFR4 in the proliferation and metastasis of colorectal cancer cells. Immunohistochemistry was used to detect the relationship between FGFR4 expression and clinicopathological features in colorectal cancer tissue.
Effect of FGFR4 silencing the tumor cell proliferation, cell cycle, apoptosis, migration and invasion were evaluated through lentiviral transfection of colorectal cancer cell line SW620. Western blot analysis used to detect changes of the epithelial-mesenchymal transition (EMT) markers, following FGFR4 silencing. FGFR4 upregulated in CRC tissues compared to normal tissues.
Patients with high FGFR4 expression exhibited a 5-year survival rate is lower compared to patients with low FGFR4 expression (64 vs 74%). FGFR4 silencing reduces proliferation, cell invasion is inhibited, the cells in S phase arrest and promoted apoptosis in colorectal cancer cells. FGFR4 silencing partially reversed the development of EMT and FGFR4 this effect is enhanced in the presence of XAV939 (inhibitor of β-catenin).
Description: CRK, also known as p38, is a protein that in humans is encoded by the CRK gene. This gene is a member of an adapter protein family that binds to several tyrosine-phosphorylated proteins. It is mapped to 17p13.3. The protein participates in the Reelin signaling cascade downstream of DAB1. The product of this gene has several SH2 and SH3 domains (src-homology domains) and is involved in several signaling pathways, recruiting cytoplasmic proteins in the vicinity of tyrosine kinase through SH2-phosphotyrosine interaction. The N-terminal SH2 domain of Crk functions as a positive regulator of transformation whereas the C-terminal SH3 domain functions as a negative regulator of transformation. Two alternative transcripts encoding different isoforms with distinct biological activity have been described.
Current data indicate that FGFR4 may be associated with prognosis in patients with colorectal cancer. In vitro functional tests reveal that the FGFR4 may represent an effective therapeutic target for colorectal cancer. FGFR4 can also set an EMT through the Wnt / β-catenin.
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