Research Paper Volume 13, Issue 7 pp 9766—9779
lncRNA OGFRP1 promotes tumor progression by activating the AKT/mTOR pathway in human gastric cancer
- 1 Department of Oncology, Lianyungang Clinical College of Nanjing Medical University, The First People’s Hospital of Lianyungang, Lianyungang, China
- 2 Department of Radiation Oncology, Lianyungang Second People's Hospital, Lianyungang, China
- 3 Department of General Surgery, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, China
- 4 Deparment of Oncology, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China
Received: November 19, 2019 Accepted: October 20, 2020 Published: March 19, 2021
https://doi.org/10.18632/aging.202731How to Cite
Copyright: © 2021 Zhang 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
As biomolecules of great clinical value, lncRNAs play a crucial role as regulators in the processes of tumor origin, metastasis, and recurrence. Thus, lncRNAs are urgently needed for research in gastric cancer. We elucidated the specific function of OGFRP1, both in vitro and in vivo. OGFRP1 was expressed at abnormally high levels in gastric cancer samples (n = 408) compared to normal samples (n = 211). Similar results were obtained in 30 clinical case samples. Interference of OGFRP1 markedly blocked cell proliferation and migration, and it induced cell cycle arrest and the apoptosis of gastric cancer cells in vitro. Phosphorylation of AKT was inhibited in cells transfected with OGFRP1 siRNA, as compared to their control cells. The in vivo results further confirmed the antitumor effects of OGFRP1 knockdown on gastric cancer. Decreases in tumor volume (104.23±62.27 mm3) and weight (0.1006±0.0488 g) in nude mice were observed during the OGFRP1 interference, as compared with the control group (418.96±211.96 mm3 and 0.2741±0.0769 g). OGFRP1 promotes tumor progression through activating the AKT/mTOR pathway. Our findings provide a new potential target for the clinical treatment of human gastric cancer.