J Song1, Q-Y Wei. 1. Department of Geriatrics, DaLian Friendship Hospital, Dalian, China. weiqingyu1964@163.com.
Abstract
OBJECTIVE: Non-small cell lung cancer (NSCLC) is one of the most ordinary cancers worldwide. Recent studies have discovered many oncogenes play vital roles in the tumorigenesis of malignant tumors. The purpose of our study was to uncover the role of GBP1 in NSCLC and the underlying mechanism. PATIENTS AND METHODS: GBP1 expression in NSCLC samples was detected by Real Time quantitative-Polymerase Chain Reaction (RT-qPCR). Function assays were performed in NSCLC cells transfected with GBP1 shRNA. Furthermore, RT-qPCR and Western blot assay were conducted to explore the target signaling pathway of GBP1. RESULTS: GBP1 expression was significantly upregulated in NSCLC tissue samples compared with adjacent normal tissues. Function assays showed that the proliferation of NSCLC cells was significantly inhibited via knockdown of GBP1, while cell apoptosis was promoted. Resistance to paclitaxel was reversed after GBP1 knockdown in paclitaxel resistance A549 cells (A549/Taxol). In addition, Wnt/β-catenin signaling pathway was repressed via knockdown of GBP1 in NSCLC cells and A549/Taxol cells. CONCLUSIONS: In our study, GBP1 was firstly identified as a novel oncogene in NSCLC. Furthermore, it could promote NSCLC development and paclitaxel resistance by inducing Wnt/β-catenin signaling pathway.
OBJECTIVE:Non-small cell lung cancer (NSCLC) is one of the most ordinary cancers worldwide. Recent studies have discovered many oncogenes play vital roles in the tumorigenesis of malignant tumors. The purpose of our study was to uncover the role of GBP1 in NSCLC and the underlying mechanism. PATIENTS AND METHODS: GBP1 expression in NSCLC samples was detected by Real Time quantitative-Polymerase Chain Reaction (RT-qPCR). Function assays were performed in NSCLC cells transfected with GBP1 shRNA. Furthermore, RT-qPCR and Western blot assay were conducted to explore the target signaling pathway of GBP1. RESULTS:GBP1 expression was significantly upregulated in NSCLC tissue samples compared with adjacent normal tissues. Function assays showed that the proliferation of NSCLC cells was significantly inhibited via knockdown of GBP1, while cell apoptosis was promoted. Resistance to paclitaxel was reversed after GBP1 knockdown in paclitaxel resistance A549 cells (A549/Taxol). In addition, Wnt/β-catenin signaling pathway was repressed via knockdown of GBP1 in NSCLC cells and A549/Taxol cells. CONCLUSIONS: In our study, GBP1 was firstly identified as a novel oncogene in NSCLC. Furthermore, it could promote NSCLC development and paclitaxel resistance by inducing Wnt/β-catenin signaling pathway.