Research Paper Volume 12, Issue 14 pp 14452—14466
Long noncoding RNA LINC01559 promotes pancreatic cancer progression by acting as a competing endogenous RNA of miR-1343-3p to upregulate RAF1 expression
- 1 Department of Osteology, The First Peoples Hospital of Neijiang, Neijiang, Sichuan, China
- 2 Department of Hepatic-Biliary-Pancreatic Surgery, The First Peoples Hospital of Neijiang, Neijiang, Sichuan, China
- 3 Department of Gastroenterology, The First Peoples Hospital of Neijiang, Neijiang, Sichuan, China
Received: March 6, 2020 Accepted: May 27, 2020 Published: July 17, 2020
https://doi.org/10.18632/aging.103487How to Cite
Abstract
Background: An increasing number of studies have shown that lncRNAs are involved in the biological processes of pancreatic cancer (PC). Hence, we investigated the role of a novel noncoding RNA, LINC01559, involved in PC progression.
Results: LINC01559 and RAF1 were highly expressed in PC, while miR-1343-3p had low expression. High expression of LINC01559 was significantly associated with large tumors, lymph node metastasis, and poor prognosis. Functional experiment results revealed that silencing of LINC01559 significantly suppressed PC cell proliferation and metastasis. Meanwhile, LINC01559 could act as a ceRNA to competitively sponge miR-1343-3p to up-regulate RAF1 and activate its downstream ERK pathway
Conclusions: LINC01559 functions as an oncogene in PC progression through acting as a ceRNA of miR-1343-3p. Hence, LINC01559 is a potential diagnostic and therapeutic target.
Methods: RT-qPCR was performed to determine the expression of LINC01559 and miR-1343-3p in PC. Individual patient data were collected to investigate the correlation between clinicopathological features and LINC01559 expression. Subsequently, the expression of LINC01559, miR-1343-3p, and RAF1 was altered using transfection of vectors or inhibitors. Gain- and loss-of-function assays and mechanistic assays were applied to verify the effects of LINC01559, miR-1343-3p, and RAF1 on PC cell proliferation and metastasis in vivo and in vitro.