食管腺癌与Barrett食管基因表达谱的研究(英文)

Objective: The aim of this study was to investigate the characteristics of gene changes from Barrett’s esophagus (BE) to esophageal adenocarcinoma by cDNA microarray. Methods: The cDNA retro-transcribed from equal quantity mRNA from esophageal carcinoma and BE tissues as well as control normal epithelium of esophagus which were from one patient with esophageal adenocarcinoma were labeled with Cy5 and Cy3 fluorescence as probes. The mixed probes were hybridized with two pieces gene chip respectively. It was scanned by laser scanner Scan Array 4000. The acquired images were analyzed by software GenePix Pro 3.0. Results: A total of 214 genes were screened out which expression levels were more than 2 times in hybridization of esophageal adenocarcinoma vs normal epithelium of esophagus, whereas 90 genes in hybridization of BE vs normal epithelium. A parallel comparison among these two gene profiles showed that a total of 45 genes with 24 downregulation and 21 up-regulation which expression levels were more than 2 times between the BE and the esophageal adenocarcinoma. Among these, there were 27 genes with 18 downregulation and 9 up-regulation which implicated the tendencies progressing from BE to esophageal adenocarcinoma. Conclusion: These genes or their products which implicate the tendencies can be chosen as indicators of carcinogenesis with high risk index for BE.

Effect of microRNA-143-3p-mediated CTNND1 on the biological function of lung cancer cells

Lung cancer poses a serious threat to human life with high incidence and miRNA is an important biomarkerin tumors. This study aimed to explore the effect of miR-143-3p on the biological function of lung cancer cells and theunderlying mechanism. Eighty-seven samples of lung cancer tissues and 81 samples of tumor-adjacent tissues from patients undergoing radical lung cancer surgery in our hospital were collected. The lung cancer cells and lung fibroblastcells (HFL-1) were purchased, and then miR-143-3p-mimics, miR-NC, si-CTNND1, and NC were transfected into A549 and PC-9 cells to establish cell models. MiR-143-3p and CTNND1 expression levels were measured by the qRT-PCR, Bax, Bcl-2, and CTNND1 expression levels by the Western Blot (WB), and cell proliferation, invasion, and apoptosis by the MTT assay, Transwell assay, and flow cytometry. Dual luciferase report assay was used to determinethe relationship between miR-143-3p and CTNND1. In this study, miR-143-3p was lowly expressed in lung cancer and CTNND1 was highly expressed in lung cancer. The overexpression of miR-143-3p inhibited cell proliferation and invasion, promoted cell apoptosis, significantly increased Bax protein expression, and decreased Bcl-2 protein expression. The inhibition of CTNND1 led to opposite biological characteristic in cells. The dual luciferase reporter assay demonstrated that miR-143-3p was a target region of CTNND1. Such results suggest that miR-143-3p can inhibitthe proliferation and invasion of lung cancer cells by regulating the expression of CTNND1 and promote the apoptosisof lung cancer cells, sott is expected to be a potential target for lung cancer.