ABSTRACT
@#Objective: To detect the expression of non-coding RNA snord105b in gastric cancer (GC) tissues, sera and cell lines, and its correlation with clinicopathological characteristics of patients with GC as well as its effect on the proliferation of GC cells. Methods: One hundred and twenty pairs of GC tissues and corresponding para-cancerous tissues from patients, who underwent surgery at Department of Surgery, the Fourth Hospital of Hebei Medical University between 2016 and 2017, were collected for this study. The presurgical sera samples from GC patients (n=50) and peripheral venous blood samples from healthy donors (n=30), as well as five gastric cancer cell lines (SGC-7901, AGS, MGC-803, BGC-823, HGC-27) and gastric mucosa normal epithelial GES-1 cells were also obtained. qPCR assay was adopted to detect the expression of snord105b in GC tissues, sera and cell lines. The correlation between snord105b and patients’clinicopathological features was investigated. MTS assay was adopted to detect the effect of snord105b silence or over-expressionon in vitro proliferation of four GC cells. Results: qPCR assay demonstrated that the expression of snord105b in GC tissues, sera and cell lines were significantly higher than that of para-cancerous tissues, sera from healthy donors and GES-1 cells (all P< 0.05). Expression level of snord105b was obviously associated with age,tumor size, differentiation and TNM stages of patients (all P<0.05). MTS assay demonstrated that knockdown of snord105b could suppress the proliferation of GC cells (P< 0.05), while forced-expression of snord105b could promote the proliferation of GC cells (P< 0.05). Conclusion: non-coding RNA snord105b aberrantly expressed in GC tissues, sera, and cells, and its expression was obviously correlated with patients’age, tumor size, differentiation and TNM stages. Snord105b could significantly promote the proliferation of GC cells, which may be used as a potential clinical biomaker for early diagnosis and prognosis of GC.
ABSTRACT
@# Objective: To investigate the expression of miR-1269 in non-small-cell lung cancer (NSCLC) tissues, and to explore its effect on the cellular biological characteristics of NSCLC A549 cells and the underlying mechanism. Methods: 34 pairs of NSCLC tissues and the corresponding adjacent para-cancerous tissues obtained from the patients, who underwent surgery in the Department of Breast Surgery, the Fourth Hospital of Hebei Medical University from Jan. 2017 to Jan. 2018, were collected for this study. The expression level of miR-1269 in above tissue specimens was examined by real-time fluorescent quantitative PCR.After transfection with miR1269 mimics and mimics NC (negative control), the proliferation, migration and invasion of A549 cells were detected by MTS, Wound healing and Transwell assay, respectively; and the changes in cell cycle distribution of A549 cells were examined by flow cytometry. The bioinformatics tool was used to predict the possible target gene of miR-1269, and the regulation effect of miR-1269 on target gene was then validated by Western blotting and Dual-luciferase reporter assay. In the meanwhile, the protein expressions of cyclin depen dent kinase inhibitor p21, Cyclin D2, and EMT-related proteins (E-cadherin and ZEB2) in the transfected A549 cells were measured by Western blotting. Results: The expression level of miR-1269 in NSCLC tissues was significantly higher than that in paracancerous tissues (2.81±2.27 vs 1.61±1.36, P <0.05). The capacities of proliferation, migration and invasion ofA549 cells in miR-1269 mimics transfection group were significantly higher than those in mimics NC group and blank control group (all P <0.01). And the cell proportion at S-phase in miR-1269-mimics group was obviously higher than that in mimics NC group [(46.54±1.57)% vs (23.32±3.15)%， P<0.01]. Bioinformatics analysis showed that miR-1269 could combine with 3’UTR of FOXO1 gene. After transfection with miR-1269 mimics, the expression level and luciferase activity of FOXO1 protein in A549 cells were significantly reduced (all P <0.01). Moreover, the protein expressions of p21 and E-cadherin were significantly decreased after over-expression of miR-1269 (all P <0.05), while the expressions of ZEB2 and Cyclin D2 were up-regulated (all P <0.05). Conclusion: The expression level of miR-1269 in NSCLC tissues was significantly increased, and it could enhance the proliferation, cell cycle progression, migration and invasion ofA549 cells. The possible mechanism may be related to its targeted regulation of FOXO1.