Research Paper Volume 12, Issue 11 pp 10517—10526
LncRNA SOCS2-AS1 inhibits progression and metastasis of colorectal cancer through stabilizing SOCS2 and sponging miR-1264
- 1 Department of Colorectal and Anal Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
- 2 Department of Vascular Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
- 3 Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
Received: March 6, 2020 Accepted: April 20, 2020 Published: May 21, 2020
https://doi.org/10.18632/aging.103276How to Cite
Copyright © 2020 Zheng 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.
Abstract
Abnormal expression of long noncoding RNA (lncRNA) is involved in human cancers, including colorectal cancer (CRC). However, their functional mechanism is largely unknown. In this study, we explored the roles of lncRNA SOCS2-AS1 in modulating CRC progression. We showed that SOCS2-AS1 was lowly expressed in CRC tissues and cells. SOCS2-AS1 downregulation predicted a poor prognosis in patients with CRC. SOCS2-AS1 overexpression significantly suppressed CRC cell proliferation, colony formation, EdU incorporation, cell-cycle, migration and invasion in vitro while SOCS2-AS1 knockdown led to an opposite phenotype. SOCS2-AS1 overexpression inhibited CRC growth and metastasis in vivo. Mechanistically, we discovered that SOCS2-AS1 was positively correlated with SOCS2 expression in CRC tissues. SOCS2-AS1 contributes to SOCS2 expression through restraining miR-1264. Additionally, we showed that SOCS2 silencing abrogated the suppressive effects of SOCS2-AS1 overexpression. Taken together, our results identified a novel regulatory loop in which SOCS2-AS1/miR-1264/SOCS2 axis suppresses CRC progression.