ISSN: 1837-9664Journal of Cancer
Global reach, higher impact
J Cancer 2019; 10(25):6405-6413. doi:10.7150/jca.32216 This issue Cite
Research Paper
Up-regulation of LINC00467 promotes the tumourigenesis in colorectal cancer
1. Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
2. Department of Endocrinology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
3. Department of Pathology, Dezhou People's Hospital, Dezhou, Shandong 253056, China
4. Department of Orthopedics, The First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China.
5. Department of Oncology, Xiangya Hospital, Central South University,Changsha, Hunan 410008, China.
6. Department of Hematology, Xiangya hospital, Central South University, Changsha, Hunan 410008, China.
7. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China.
*These authors jointly supervised this work.
Abstract
Recent studies have reported that long non-coding RNAs (lncRNAs) are associated with the tumourigenesis of colorectal cancer (CRC); however, several of these are yet to be identified and characterised. In this study, we report a novel lncRNA, LINC00467, which was significantly up-regulated in CRC; we investigated its function and mechanism in CRC. Our study demonstrated that LINC00467 levels in 45 pairs of CRC tissues were higher than those in the corresponding normal colon mucosal tissues. We used the Gene Expression Omnibus (GEO) and Gene Expression Profiling Interactive Analysis (GEPIA) databases for the analysis and measurement of clinical samples, and observed that the CRC patients with high LINC00467 expression levels showed poor overall survival (OS) and recurrent-free survival (RFS) rates. Furthermore, following the short interfering RNA (siRNA) knockdown of LINC00467 in the CRC cell line, the results demonstrated that LINC00467 suppresses the proliferation, invasion and metastasis of CRC cells in vitro. Moreover, its molecular mechanism of LINC00467 decreased the expression of Cyclin D1, Cyclin A1, CDK2, CDK4 and Twist1 as well as enhanced the expression of E‑cadherin. Collectively, these findings suggest that LINC00467 may be crucial in the progression and development of CRC, and may serve as a potential therapeutic target for CRC patients.
Keywords: LINC00467, colorectal cancer, tumorigenesis, invasion, survival
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