MiR-27a-3p promotes esophageal cancer cell proliferation via F-box and WD repeat domain-containing 7 (FBXW7) suppression.

Emerging evidence has suggested that dysregulation of microRNA-27a-3p (miR-27a-3p) may contribute to tumor development and progression in various types of cancers. However, its role in esophageal cancer is still unknown. In the present study, miR-27a-3p was significantly increased in esophageal squamous cell carcinoma (ESCC) tissues and cell lines. In esophageal cancer Eca109 cells, ectopic overexpression of miR-27a-3p promoted cell proliferation, meanwhile, cell proliferation was reduced by miR-27a-3p inhibition. Further studies showed that down-regulated miR-27a-3p expression could induced cell cycle arrest at the G1/S transition. In exploring mechanisms underlying the promotive role, our results revealed that miR-27a-3p markedly inhibited the expression of F-box and WD repeat domain-containing 7 (FBXW7). FBXW7, a tumor suppressor, exhibited significantly inhibitory effect on Eca109 cell proliferation. Thus our observations suggested that miR-27a-3p functioned as a tumor suppressor by targeting FBXW7. These findings indicated that miR-27a-3p could be considered as a potential therapeutic strategy for ESCC therapy.

Increased expression and function of P-glycoprotein in peripheral blood CD56+ cells is associated with the chemoresistance of non-small-cell lung cancer.

PURPOSE: Chemoresistance is common among non-small-cell lung cancer (NSCLC), P-glycoprotein (P-gp), encoded by the human multi-drug-resistant MDR1 gene, and multidrug-resistance protein 1 (MRP1) might be major contributors. The aim of the present study was to develop an effective method to investigate the expression and function of P-gp in the peripheral CD56+ cells in order to clarify their correlation with the chemoresistance in NSCLC. METHODS: Using microbead technology and a RT-qPCR methodology, we evaluated the expression levels of P-gp and MRP1 in the purified CD56+ cells in the chemoresistance and chemo-naive NSCLC patients compared with that in the healthy volunteers. Flow cytometric analysis was used to investigate the changes of P-gp function in the CD56+ cells between the three cohorts. RESULTS: The MDR1 gene expression was elevated markedly (twofold-tenfold), and P-gp function was increased in the chemoresistance cohort compared with the chemo-naive and the healthy cohorts; whereas there was only about two times averagely elevated for the MRP1 gene expression. No statistical significance (p > 0.05) was seen with respect to the expression of MDR1 and MRP1, the function of P-gp between the chemo-naive and the healthy cohorts. CONCLUSIONS: P-gp in peripheral CD56+ cells demonstrated possible clinical relevance as predictive biomarkers for the identification of chemoresistance in NSCLC, while MRP1 may not play a significant role in the drug resistance in NSCLC. The potential applications for this finding are provided evidence to screen the potential P-gp reversors and to diagnose and manage the chemoresistance in NSCLC patients.