Yuqi Luo1,2, Jun Ouyang3, Donggen Zhou4, Shizhen Zhong1, Minjie Wen2, Wentao Ou2, Haitao Yu2, Lin Jia5, Yaoxin Huang5. 1. Department of Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China. 2. Department of General Surgery, Nansha Hospital of Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 511457, China. 3. Department of Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China. jouyang@126.com. 4. Ningbo international Travel Healthcare Center, Ningbo, 315000, China. 5. Department of Gastroenterology, Nansha Hospital of Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 511457, China.
Abstract
BACKGROUND: Gastric adenocarcinoma predictive long intergenic noncoding RNA (GAPLINC) has been detected in colorectal cancer (CRC) cells and reportedly performs many functions related to tumor proliferation and metastasis. Aim The present study aimed to comprehensively explore the biological functions of GAPLINC and their underlying mechanism in CRC cell. METHODS: The human cancer LncRNA PCR array was used to detect the differentially expressed long noncoding RNAs in human CRC samples. Real-time PCR, dual-luciferase assay, RNA pull-down assay, Transwell assay, and western blot analysis were performed to explore the molecular mechanism underlying GAPLINC functions related to migration and invasion of a human CRC cell line (HCT116). RESULTS: Compared to the non-cancerous tissues, GAPLINC expression was obviously increased in CRC tissues. In HCT116, silencing of GAPLINC weakened cell migration and invasion, while overexpression of GAPLINC significantly promoted cell migration and invasion. Through dual-luciferase, RNA pull-down, and Transwell assays, we verified that miR-34a was the downstream molecule of GAPLINC and that miR-34a negatively regulated the migration and invasion of HCT116 cell. Furthermore, we found that GAPLINC positively regulated the miR-34a target gene c-MET in CRC tissues. CONCLUSIONS: Our findings revealed that GAPLINC was up-regulated in CRC tissues and was involved in the migration and invasion of CRC cells by regulating miR-34a/c-MET signaling pathway.
BACKGROUND:Gastric adenocarcinoma predictive long intergenic noncoding RNA (GAPLINC) has been detected in colorectal cancer (CRC) cells and reportedly performs many functions related to tumor proliferation and metastasis. Aim The present study aimed to comprehensively explore the biological functions of GAPLINC and their underlying mechanism in CRC cell. METHODS: The humancancer LncRNA PCR array was used to detect the differentially expressed long noncoding RNAs in human CRC samples. Real-time PCR, dual-luciferase assay, RNA pull-down assay, Transwell assay, and western blot analysis were performed to explore the molecular mechanism underlying GAPLINC functions related to migration and invasion of a human CRC cell line (HCT116). RESULTS: Compared to the non-cancerous tissues, GAPLINC expression was obviously increased in CRC tissues. In HCT116, silencing of GAPLINC weakened cell migration and invasion, while overexpression of GAPLINC significantly promoted cell migration and invasion. Through dual-luciferase, RNA pull-down, and Transwell assays, we verified that miR-34a was the downstream molecule of GAPLINC and that miR-34a negatively regulated the migration and invasion of HCT116 cell. Furthermore, we found that GAPLINC positively regulated the miR-34a target gene c-MET in CRC tissues. CONCLUSIONS: Our findings revealed that GAPLINC was up-regulated in CRC tissues and was involved in the migration and invasion of CRC cells by regulating miR-34a/c-MET signaling pathway.
Authors: Seonhoe Kim; Ui Jin Lee; Mi Na Kim; Eun-Ju Lee; Ji Young Kim; Mi Young Lee; Sorim Choung; Young Joo Kim; Young-Chul Choi Journal: J Biol Chem Date: 2008-05-02 Impact factor: 5.157
Authors: Thomas Schweiger; Veronika Starkl; Olaf Glueck; Christoph Glogner; Denise Traxler; Julia Jedamzik; Sandra Liebmann-Reindl; Peter Birner; Berthold Streubel; Walter Klepetko; Konrad Hoetzenecker Journal: Eur J Cardiothorac Surg Date: 2015-10-24 Impact factor: 4.191