Research Paper Volume 12, Issue 6 pp 5183—5194
LncRNA AGAP2-AS1 augments cell viability and mobility, and confers gemcitabine resistance by inhibiting miR-497 in colorectal cancer
- 1 Department of Colorectal and Anal Surgery, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China
- 2 Department of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin Province, China
- 3 Department of Thoracic Oncology, Tumor Hospital of Jilin Province, Changchun 130000, Jilin Province, China
- 4 Department of Ophthalmology, The China-Japan Union Hospital of Jilin University, Jilin University, Changchun 130033, Jilin Province, China
received: November 13, 2019 ; accepted: January 27, 2020 ; published: March 23, 2020 ;https://doi.org/10.18632/aging.102940
How to Cite
Copyright © 2020 Hong et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Most recently, long non-coding RNAs (lncRNAs) emerge as crucial modulators in many biological processes, such as embryonic development, cell growth, and tumorigenesis. However, the correlations between lncRNAs and colorectal cancer (CRC) cell proliferation, metastasis, and gemcitabine resistance are not well understood.
Results: The expression of AGAP2-AS1 was overexpressed in CRC tissues and negatively correlated with the survival of patients with CRC. AGAP2-AS1 promoted CRC cell proliferation and inhibited apoptosis. Moreover, AGAP2-AS1 enhanced the chemoresistance of CRC cells to gemcitabine. In addition, AGAP2-AS1 enhanced the migration and invasion of CRC cells. Mechanistic studies showed that AGAP2-AS1 regulated fibroblast growth factor receptor 1 (FGFR1) expression by sponging miR-497 in CRC progression.
Conclusion: We identified an oncogenic role of AGAP2-AS1 in the development and progression of CRC.
Methods: qRT-PCR was used to measure the expression of AGAP2 Antisense RNA 1 (AGAP2-AS1) in 116 cases of CRC and adjacent normal tissues. Luciferase reporter assays was used to detect the interaction between AGAP2-AS1 and miR-497. The xenograft tumor experiment was used to study the in vivo function of AGAP2-AS1.