Sichuan Da Xue Xue Bao Yi Xue Ban
September 2020
Objective: To examine copper transporter 1 (CTR1) expression in pancreatic carcinoma cells, orthotopic xenograft pancreatic tumor model and clinical samples, and verify the effect of copper chelating agent ammonium tetrathiomolybdate (TM) regulate the expression of CTR1 in pancreatic carcinoma cells and the inhibition of pancreatic carcinoma.
Methods: The expressions of copper transporter CTR1 and antioxidant protein 1 (ATOX1) in 22 clinical pancreatic ductal carcinoma and paracancer tissues 0.5-1 cm away from the tumor were measured by immunohistochemistry (IHC).
Objective: To study the effect of methylation level of microRNA promoter on the expression of microRNAs (miRNA34a, miRNA34b, miRNA148a, miRNA203a) and on the proliferation, migration and invasion of lung cancer A549 cells.
Methods: The proliferation of A549 cells treated with different concentrations of demethylated drug 5-aza-2'-deoxycytidine (5-Aza-CdR) was measured by CCK8 assay and calculated the inhibitory rate in 24 h, 48 h and 72 h, respectively. After 72 h of treatment with 20 μmol/L 5-Aza-CdR, methylation-specific PCR (MSP) was used to detect the methylation level of A549 cells in miRNAs gene promoter regions, and real-time quantitative PCR (real-time PCR) was used to test the expression of miRNAs.
Sichuan Da Xue Xue Bao Yi Xue Ban
November 2017
Objective: To study the epigenetic regulation of pancreatic carcinoma related microRNA (miR34a,miR34b,miR148a and miR203a) expression by gene promoter methylation,and its effect on the proliferation,migration and invasion of pancreatic carcinoma cells.
Methods: The pancreatic carcinoma cells were divided into two groups:control group and treatment group.Control group was treated with 0 μmol/L DNA methyltransferase inhibitor 5-Aza-CdR and treatment group was treated with 60 μmol/L 5-Aza-CdR.
Objectives: To study the regulation to colon cancer cellular biological properties through miR-18a targeting ataxia-telangiectasia mutated gene ().
Methods: A target of miR-18a was predicted by using bioinformatics tools. The miR-18a mimics and inhibitors were designed and synthesized.