Loading…

LncRNA LINC01857 drives pancreatic adenocarcinoma progression via modulating miR-19a-3p/SMOC2

•LINC01857 is upregulated in PAAD and promotes malignant cellular behaviors.•LINC01857 interacts with miR-19a-3p to regulate SMOC2 expression.•LINC01857 promotes malignant cellular phenotypes by upregulating SMOC2. Emerging evidence has demonstrated that LINC01857 exerts a pivotal function in many c...

Full description

Saved in:
Bibliographic Details
Published in:Clinics (São Paulo, Brazil) Brazil), 2022-01, Vol.77, p.100047-100047, Article 100047
Main Authors: Lu, Yeting, Ying, Dongjian, Tian, Yuan, Ruan, Yi, Cheng, Gong, Lv, Kaiji, Zhou, Xinhua, Han, Shuo
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:•LINC01857 is upregulated in PAAD and promotes malignant cellular behaviors.•LINC01857 interacts with miR-19a-3p to regulate SMOC2 expression.•LINC01857 promotes malignant cellular phenotypes by upregulating SMOC2. Emerging evidence has demonstrated that LINC01857 exerts a pivotal function in many cancers. However, its function in Pancreatic Ductal Adenocarcinoma (PDAC) still remains unclear. This study was designed to investigate the regulatory character of LINC01857 in PDAC. Bioinformatic tools and databases were used to seek potential miRNAs and mRNAs. Gene expression was evaluated by Reverse Transcription quantitative real-time Polymerase Chain Reaction (RT-qPCR), and western blot was used for protein level detection. A subcellular fraction assay was done to ascertain the location of LINC01857 in PANC-1 and BxPC-3 human pancreatic cancer cells. CCK-8, EdU, wound healing and Transwell assays were performed to inquire into the influence of LINC01857, and SPARC -related Modular Calcium-binding protein-2 (SMOC2) on cell viability, proliferation, migration, and invasion, respectively. The interaction between LINC01857 and its downstream genes was explored by RNA immunoprecipitation and luciferase reporter assays. LINC01857 levels were significantly elevated in PDAC. Knockdown of LINC01857 significantly restrained the proliferation, migration, invasion, and Epithelial-Mesenchymal Transition (EMT) process of PDAC cells. MiR-19a-3p was a downstream target of LINC01857, and miR-19a-3p levels were significantly decreased in PDAC cells. In addition, SMOC2 expression had a negative correlation with that of miR-19a-3p, and SMOC2 was a downstream target of miR-19a-3p. Furthermore, SMOC2 upregulation partially abolished the inhibitive influence of LINC01857 downregulation on cell proliferation, migration, invasion, and the EMT process. LINC01857 promotes malignant phenotypes of PDAC cells via upregulation of SMOC2 by interacting with miR-19a-3p.
ISSN:1807-5932
1980-5322
1980-5322
DOI:10.1016/j.clinsp.2022.100047