Wei Zong1, Wei Feng1, Yun Jiang1, Yaning Cao2, Yuchen Ke2, Xin Shi1, Shaoqing Ju1, Hui Cong1, Xudong Wang1, Ming Cui3, Rongrong Jing4. 1. Department of Laboratory Medicine, Affiliated Hospital of Nantong University, No 20, Xisi Road, Nantong, 226001, China. 2. School of Public Health, Nantong University, Nantong, China. 3. Department of Laboratory Medicine, Affiliated Hospital of Nantong University, No 20, Xisi Road, Nantong, 226001, China. wscm163@163.com. 4. Department of Laboratory Medicine, Affiliated Hospital of Nantong University, No 20, Xisi Road, Nantong, 226001, China. jrjr2020@163.com.
Abstract
BACKGROUND: Long non-coding RNAs (lncRNAs) have emerged as important roles in gastric cancer (GC). However, the role of the dysregulated lncRNAs in GC remained large unknown. We investigated the clinical significance, biological function and mechanism of CTC-497E21.4 in GC. METHODS: Firstly, RTFQ-PCR was used to detect the expression of CTC-497E21.4 in GC. Furthermore, knockdown of CTC-497E21.4 was conducted to assess the effect of CTC-497E21.4 in vitro and vivo. Subcellular localization of CTC-497E21.4 was determined by nuclear plasmolysis PCR and FISH. We also predicted CTC-497E21.4 binding miRNAs and downstream target genes and evaluated its regulation of miR-22 by acting as a ceRNA. RESULT: CTC-497E21.4 was upregulated in GC tissues and GC cell lines (P < 0.05), and the expression was associated with depth of invasion, lymph node metastasis, and neurological invasion. Besides, knockdown of CTC-497E21.4 inhibited cell proliferation, invasion and promoted cell cycle arrest in vitro and inhibited tumorigenesis in vivo. Mechanistic investigations indicated that CTC-497E21.4 acted as a ceRNA for miR-22 and regulated NET1 expression. CTC-497E21.4/miR-22-3p/NET1 participated in the RhoA signaling pathway in the GC progression. CONCLUSION: CTC-497E21.4 competed with miR-22 to regulate the expression of NET1 and regulated the malignant progression of GC through RhoA signaling pathway.
BACKGROUND: Long non-coding RNAs (lncRNAs) have emerged as important roles in gastric cancer (GC). However, the role of the dysregulated lncRNAs in GC remained large unknown. We investigated the clinical significance, biological function and mechanism of CTC-497E21.4 in GC. METHODS: Firstly, RTFQ-PCR was used to detect the expression of CTC-497E21.4 in GC. Furthermore, knockdown of CTC-497E21.4 was conducted to assess the effect of CTC-497E21.4 in vitro and vivo. Subcellular localization of CTC-497E21.4 was determined by nuclear plasmolysis PCR and FISH. We also predicted CTC-497E21.4 binding miRNAs and downstream target genes and evaluated its regulation of miR-22 by acting as a ceRNA. RESULT: CTC-497E21.4 was upregulated in GC tissues and GC cell lines (P < 0.05), and the expression was associated with depth of invasion, lymph node metastasis, and neurological invasion. Besides, knockdown of CTC-497E21.4 inhibited cell proliferation, invasion and promoted cell cycle arrest in vitro and inhibited tumorigenesis in vivo. Mechanistic investigations indicated that CTC-497E21.4 acted as a ceRNA for miR-22 and regulated NET1 expression. CTC-497E21.4/miR-22-3p/NET1 participated in the RhoA signaling pathway in the GC progression. CONCLUSION: CTC-497E21.4 competed with miR-22 to regulate the expression of NET1 and regulated the malignant progression of GC through RhoA signaling pathway.
Authors: Ming Sun; Fengqi Nie; Yunfei Wang; Zhihong Zhang; Jiakai Hou; Dandan He; Min Xie; Lin Xu; Wei De; Zhaoxia Wang; Jun Wang Journal: Cancer Res Date: 2016-09-20 Impact factor: 12.701