B Chen1, C-H Ling. 1. Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China. linchunhua88@hotmail.com.
Abstract
OBJECTIVE: Recent researches have proved that long noncoding RNAs (lncRNAs) play an important role in multiple diseases, including malignant tumors. The aim of this study was to explore the exact role of lncRNA AK027294 in the development of non-small cell lung cancer (NSCLC), and to investigate the possible underlying mechanism. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect the AK027294 expression in NSCLC patients. Then, cell counting kit-8 (CCK-8) assay, colony formation assay, and 5-Ethynyl-2'-deoxyuridine (EdU) incorporation assay were performed, respectively. Furthermore, RT-qPCR and Western blot assay were used to explore the potential mechanism. RESULTS: The expression level of AK027294 NSCLC samples was significantly higher than that of adjacent tissues. Subsequent functional assays showed that the growth ability of NSCLC cells was markedly inhibited after AK027294 silence. In addition, after AK027294 knock-down, the expression of signal transducers and activators of transcription 3 (STAT3) was remarkably down-regulated. Furthermore, the results demonstrated that the STAT3 expression was positively correlated with the AK027294 expression in NSCLC tissues. CONCLUSIONS: The above results indicated that AK027294 could enhance the growth ability of NSCLC by up-regulating STAT3. Our findings suggested that AK027294 might be a potential therapeutic target for NSCLC.
OBJECTIVE: Recent researches have proved that long noncoding RNAs (lncRNAs) play an important role in multiple diseases, including malignant tumors. The aim of this study was to explore the exact role of lncRNA AK027294 in the development of non-small cell lung cancer (NSCLC), and to investigate the possible underlying mechanism. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect the AK027294 expression in NSCLCpatients. Then, cell counting kit-8 (CCK-8) assay, colony formation assay, and 5-Ethynyl-2'-deoxyuridine (EdU) incorporation assay were performed, respectively. Furthermore, RT-qPCR and Western blot assay were used to explore the potential mechanism. RESULTS: The expression level of AK027294 NSCLC samples was significantly higher than that of adjacent tissues. Subsequent functional assays showed that the growth ability of NSCLC cells was markedly inhibited after AK027294 silence. In addition, after AK027294 knock-down, the expression of signal transducers and activators of transcription 3 (STAT3) was remarkably down-regulated. Furthermore, the results demonstrated that the STAT3 expression was positively correlated with the AK027294 expression in NSCLC tissues. CONCLUSIONS: The above results indicated that AK027294 could enhance the growth ability of NSCLC by up-regulating STAT3. Our findings suggested that AK027294 might be a potential therapeutic target for NSCLC.