Research Paper Volume 13, Issue 10 pp 13571—13584
Long intergenic noncoding RNA 00665 promotes proliferation and inhibits apoptosis in colorectal cancer by regulating miR-126-5p
- 1 Department of Gastrointestinal Surgery, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250021, Shandong, People’s Republic of China
- 2 Department of Emergency Surgery, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao 262000, Shandong, People’s Republic of China
- 3 Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao 262000, Shandong, People’s Republic of China
- 4 Department of PET-CT, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao 262000, Shandong, People’s Republic of China
Received: October 26, 2020 Accepted: March 14, 2021 Published: April 20, 2021https://doi.org/10.18632/aging.202874
How to Cite
Copyright: © 2021 Wu 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.
Long intergenic noncoding RNAs (lincRNAs) regulate a series of biological processes, and their anomalous expression plays critical roles in the progression of multiple malignancies, including colorectal cancer (CRC). Although many studies have reported the oncogenic function of LINC00665 in multiple cancers, few studies have explored its role in CRC. The aim of this study was to assess the effect of LINC00665 on the malignant behaviors of CRC and explore the underlying regulatory mechanism of LINC00665. LINC00665 was significantly upregulated in CRC. A loss-of-function assay revealed that LINC00665 downregulation inhibited the proliferation and promoted the apoptosis of CRC cells, which was mediated by cyclin D1, CDK4, caspase-9 and caspase-3. Through mechanistic exploration, we found that miR-126-5p directly bound to LINC00665. Moreover, LINC00665 and miR-126-5p both regulated PAK2 and FZD3 expression. Mechanistically, miR-126-5p was predicted and further verified as a target of both PAK2 and FZD3. These findings demonstrate that LINC00665 might play an important pro-proliferative and antiapoptotic role in CRC and might be a potential biomarker and a new therapeutic target for CRC.