ABSTRACT
Aim To investigate the role and potential mechanism of methyltransferase-like 5 (METTL5) in triple-negative breast cancer (TNBC) . Methods The expression of METTL5 in TNBC tumor tissues and cell lines was detected by immunohistochemistry and Western blot. After shRNA targeting METTL5 (shRNAMETTL5) was transfected into TNBC cells, cell proliferation, migration and invasion were detected by CCK-8, colony formation, wound healing and Transwell assays, respectively. Western blot was used to detect the expression of Wnt/p-catenin signaling-related key proteins. A xenograft tumor model was constructed to verify the effect of METTL5 knockdown on the growth of TNBC cells and Wnt/p-catenin signaling activity in vivo. Results The expression of METTL5 was up-regulated in TNBC tumor tissues and cell lines (P < 0. 01) . Knockdown of METTL5 significantly inhibited the proliferation, migration and invasion of TNBC cells and reduced the expression of Wnt/p-catenin signaling molecules (3-catenin, cyclin Dl, matrix metalloproteinase (MMP) -2 and MMP-7 (all P < 0. 01) . Knockdown of METTL5 reduced tumor growth and Wnt/pcatenin signaling activity in vivo. Conclusions Knockdown of METTL5 can inhibit the proliferation, migration and invasion of TNBC cells, which may be related to the inhibition of Wnt/p-catenin signaling pathway.
ABSTRACT
Senile osteoporosis (SOP) is a systemic bone disease characterized by increased susceptibility to fractures. The pathogenesis of SOP is complex and not well understood. Currently, the rapid aging model mouse, senescence accelerated mouse prone 6 (SAMP6), is an ideal model for studying the mechanisms of SOP development and exploring its prevention and treatment. This model exhibits characteristics including increased bone fragility, degradation of bone microstructure, loss of bone matrix, and abnormal metabolism and dysfunction of bone cells, faithfully replicating the process of SOP occurrence and progression at both macroscopic and microscopic levels.
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Objective: To construct the form deprivation myopia (FDM) rat models, and to elucidate the expression of transforming growth fact or-(21 CTGF-ß1 ) in scleral fibroblasts of the FDM rats and its relationship with Wnt/p-catenin signaling pathway. Methods: Forty rats were randomly divided into control group and FDM model group, with 20 rats in each group. The FDM rat model was established in FDM model group. The axial lengths of the rats were determined. The rat sclera tissue of eyeball was separated. The expression levels of TGF-ß1 protein and mRNA in sclera tissue of the rats were determined by Western blotting and reverse transcription-polymerase chain reaction CRT-PCR) methods. The scleral fibroblasts of rats were isolated and cultured. The fibroblasts in the sclera of the rats in control group were used as the control group. The fibroblasts in FDM model group were divided into FDM group and FDM+ Dickkopf related protein 1 (DDK1) group (added to DDK 1 to culture). The expression levels of TGF-ß1. Dicer-like 3 (DCL3)» colon adenomatous polyp protein CAPO, glycogen synthase kinase 30 (GSK3{3)» p21-GSK3j3. and {3-catenin protein and mRNA in scleral fibroblasts were determined by Western blotting and RT-PCR methods. Results: Compared with control group-the axial length of the rats in FDM group was increased (P0. 05) ; but there were significant differences in the expression levels of TGF-ß1, DC 1.3. APC. p21-GSK30. and p-catenin protein and mRNA in the scleral fibroblasts C P< 0.01). Compared with control group, the expression levels of TGF-ß1 and APC protein and mRNA in scleral fibroblasts of the rats in FDM group were decreased (P<.0. 01). and the expression levels of DCL3» p21-GSK3(3. and (3-catenin protein and mRNA were increased ( P<0. 05). Compared with FDM group, the expression levels of TGF-ß1 and APC protein and mRNA in the scleral fibroblasts of the rats in FDM+DDK1 group were increased CP<0. 01). and the expression levels of DCL3. p21-GSK3,3. and 0-catenin protein and mRNA were decreased ( P< 0. 01). Conclusion: The expression level of TGF-,ß1 in the scleral fibroblasts of the FDM model rats is decreased, and its level is regulated by the Wnt. p-catenin signaling pathway.
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Objective To investigate the expression of Oct4 in liver cancer, and the interrelation of the Oct4 and Wnt/β-catenin genes in hepatocellular carcinoma( HCC) cell line HepG2. Methods RTPCR technique was used to detect the expression of Oct4 and β-Catenin in HCC specimens; RNAi was used to knock-down the expression of Oct4 in HepG2, and the change of Wnt/β-catenin related genes were detected by Real time-PCR. Results In HCC specimens, the expression of Oct4 and β-Catenin in tumor and cirrhotic liver tissues were stronger than normal liver tissues. In SiRNA Oct4 HepG2 cells, the expression of Oct4 was downregulated, and β-catenin as well as Wnt10b were in a positive correlation with Oct4, TCF3 was in negative correlation with Oct4. Clone formation and move ability of the HepG2 were downregulated. Conclusions The expression of Oct4 was higher in tumor tissues than in normal liver tissues. Silencing Oct4 by SiRNA-0ct4 in HepG2 resulted in decreased ability of clone formation and cell movement.