Xiantao Sun1, Zhimin Wang2, Weitang Yuan1. 1. Department of Colorectal Surgery, The First Affiliated Hospital and Institute of Clinical Medicine, Zhengzhou University, Zhengzhou 450052, Henan, China. 2. Department of Endocrinology, The First Affiliated Hospital and Institute of Clinical Medicine, Zhengzhou University, Zhengzhou 450052, Henan, China.
Abstract
BACKGROUND: Colorectal carcinoma (CRC) is the vital cancer mortality worldwide and the long noncoding RNAs (lncRNAs) is considered as an important biomarker. The aim of this study was to examine the influence of lncRNA-SNHG1in CRC, and explore the relationship of lncRNA-SNHG1 and CRC, and consequently find a new therapeutic target for CRC patients. METHODS: This study used 80 CRC patients and several cancer cell lines, with RNA interference technology to find the function of SNHG1. RESULTS: SNHG1 expression was higher in CRC tissue lines other than the cancer adjacent tissues. Moreover, down-regulated SNHG1 resulting in smaller tumor size and lighter tumor weight. Additionally, down-regulated SNHG1 inhibited cell migration, proliferation and colony formation, but promoted cell apoptosis. CONCLUSION: Our findings revealed that down-regulated SNHG1 could inhibit CRC tumor genesis and SNHG1 might act as an important potential therapeutic target in CRC treatment.
BACKGROUND:Colorectal carcinoma (CRC) is the vital cancer mortality worldwide and the long noncoding RNAs (lncRNAs) is considered as an important biomarker. The aim of this study was to examine the influence of lncRNA-SNHG1in CRC, and explore the relationship of lncRNA-SNHG1 and CRC, and consequently find a new therapeutic target for CRC patients. METHODS: This study used 80 CRC patients and several cancer cell lines, with RNA interference technology to find the function of SNHG1. RESULTS:SNHG1 expression was higher in CRC tissue lines other than the cancer adjacent tissues. Moreover, down-regulated SNHG1 resulting in smaller tumor size and lighter tumor weight. Additionally, down-regulated SNHG1 inhibited cell migration, proliferation and colony formation, but promoted cell apoptosis. CONCLUSION: Our findings revealed that down-regulated SNHG1 could inhibit CRC tumor genesis and SNHG1 might act as an important potential therapeutic target in CRC treatment.