Neoplasma Vol.65, No.5, p.779-789, 2018
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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 |
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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.
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Keywords: lung cancer; PICART1; apoptosis; migration; JAK2/STAT3 pathway |
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Published online: 24-Sep-2018
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Year: 2018, Volume: 65, Issue: 5 |
Page From: 779, Page To: 789 |
doi:10.4149/neo_2018_171130N778
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