X-C Lu1, H-Y Zhou, J Wu, Y Jin, X-M Yao, X-Y Wu. 1. Department of Gastroenterology, Affiliated Wujiang Hospital of Nantong University, Suzhou, China. wuxiaoying2644@sina.com.
Abstract
OBJECTIVE: Recent studies have revealed that long non-coding RNAs (lncRNAs) play a crucial role in tumor progression. Gastric cancer (GC) is one of the common types of malignancies worldwide. This study aimed to identify the exact function of lncRNA LINP1 in the progression of GC. PATIENTS AND METHODS: LINP1 expression in paired cancer tissues and adjacent normal tissues of GC patients was detected by Real-Time quantitative Polymerase Chain Reaction (RT-qPCR). The effect of LINP1 silence on proliferation and apoptosis of GC cells was detected. Meanwhile, the underlying mechanism of LINP1 function was explored by RT-qPCR and Western blot assay. Furthermore, tumor formation assay was performed to examine the ability of LINP1 in tumor formation in vivo. RESULTS: LINP1 expression was remarkably up-regulated in GC tissues compared with adjacent normal tissues. The growth ability of GC cells was significantly inhibited after silencing of LINP1 in vitro. Besides, the apoptosis of GC cells was markedly induced after silencing of LINP1. The silence of LINP1 significantly up-regulated the expression of RBM5 in GC cells. Meanwhile, RBM5 expression in GC tissues was remarkably lower than that of the adjacent normal tissues. Furthermore, tumor formation assay showed that knockdown of LINP1 markedly inhibited tumor formation in vivo. CONCLUSIONS: These results suggested that LINP1 could down-regulate RBM5. Meanwhile, LINP1 remarkably promoted growth ability and suppressed apoptosis of GC in vitro and in vivo. Our findings might provide a novel regulator and therapeutic strategy for GC patients.
OBJECTIVE: Recent studies have revealed that long non-coding RNAs (lncRNAs) play a crucial role in tumor progression. Gastric cancer (GC) is one of the common types of malignancies worldwide. This study aimed to identify the exact function of lncRNA LINP1 in the progression of GC. PATIENTS AND METHODS: LINP1 expression in paired cancer tissues and adjacent normal tissues of GCpatients was detected by Real-Time quantitative Polymerase Chain Reaction (RT-qPCR). The effect of LINP1 silence on proliferation and apoptosis of GC cells was detected. Meanwhile, the underlying mechanism of LINP1 function was explored by RT-qPCR and Western blot assay. Furthermore, tumor formation assay was performed to examine the ability of LINP1 in tumor formation in vivo. RESULTS:LINP1 expression was remarkably up-regulated in GC tissues compared with adjacent normal tissues. The growth ability of GC cells was significantly inhibited after silencing of LINP1 in vitro. Besides, the apoptosis of GC cells was markedly induced after silencing of LINP1. The silence of LINP1 significantly up-regulated the expression of RBM5 in GC cells. Meanwhile, RBM5 expression in GC tissues was remarkably lower than that of the adjacent normal tissues. Furthermore, tumor formation assay showed that knockdown of LINP1 markedly inhibited tumor formation in vivo. CONCLUSIONS: These results suggested that LINP1 could down-regulate RBM5. Meanwhile, LINP1 remarkably promoted growth ability and suppressed apoptosis of GC in vitro and in vivo. Our findings might provide a novel regulator and therapeutic strategy for GCpatients.