Journal info
|
||
Select Journal
Journals
Bratislava Medical Journal Endocrine Regulations General Physiology and Biophysics Neoplasma 2024 Ahead of print 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 2004 2003 Acta Virologica Studia Psychologica Cardiology Letters Psychológia a patopsych. dieťaťa Kovove Materialy-Metallic Materials Slovenská hudbaWebshop Cart
Your Cart is currently empty.
Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.
Neoplasma Vol.65, No.5, p.779-789, 2018 |
||
Title: Long non-coding RNA PICART1 suppresses proliferation and promotes apoptosis in lung cancer cells by inhibiting JAK2/STAT3 signaling | ||
Author: J.M. ZHAO, W. CHENG, X.G. HE, Y.L. LIU, F.F. WANG, Y.F. GAO | ||
Abstract: Lung cancer remains the most common cause of tumor-related death worldwide. Recent studies have revealed that long non-coding RNAs (lncRNAs) are involved in the development of various cancers, including lung cancer. This study investigates the molecular basis and effect of lncRNA PICART1 on lung cancer. We first assessed the PICART1 expression in lung cancer in vitro and vivo by qRT-PCR. Then the expression of PICART1 in SPC-A-1 and NCI-H1975 cell lines was inhibited and over-expressed by transient transfections. Thereafter, cell viability, cell cycle, migration and apoptosis were measured by MTT, Transwell and flow cytometry assay. qRT-PCR and western blot analysis were then performed to assess the expression levels of apoptosis- and migration-related proteins and the JAK2/STAT3 pathway proteins. Tumor formation was measured by xenograft tumor model assay in vivo. PICART1 expression was down-regulated in human lung cancer tissues and cell lines. While PICART1 knockdown increased cell viability of lung cancer cell lines, its over-expression inhibited cell cycle progression and promoted apoptosis in SPC-A-1 and NCI-H1975 cell lines. PICART1 over-expression also inhibited migration in up-regulation of E-cadherin, and down-regulation of Twist1, MMP2 and MMP9. We also found that PICART1 inhibition can regulate cell apoptosis and migration by activating the JAK2/STAT3 pathway, and in vivo experiments revealed that PICART1 knockdown significantly promoted tumor formation. This study demonstrates that PICART1 over-expression has an anti-growth and anti-metastasis role in lung cancer cells and its tumor suppression may be via regulation of the JAK2/STAT3 pathway. |
||
Keywords: lung cancer; PICART1; apoptosis; migration; JAK2/STAT3 pathway | ||
Published online: 24-Sep-2018 | ||
Year: 2018, Volume: 65, Issue: 5 | Page From: 779, Page To: 789 | |
doi:10.4149/neo_2018_171130N778 |
||
|
download file |
|