Abstract
Background: Long noncoding RNAs (lncRNAs) have been consistently demonstrated to be involved in gastric cancer (GC) as either tumor oncogenes or tumor suppressors. However, the detailed role of MIAT in GC remains poorly understood. Methods: The expression of MIAT in GC
tissues was measured by In situ hybridization (ISH) assay. Cell proliferation, apoptosis, cycle, migration and invasion assays were performed to analyze the biological functions of MIAT in GC cells. Besides, western blotting was used to evaluate the role of MIAT in the expressions of
P16, COX-2 and MMP-9. Results: In the present study, we identified that MIAT was up-regulated in GC tissues. Furthermore, silencing MIAT significantly suppressed GC cells proliferation, migration and invasion, promoted GC cells apoptosis, and induced GC cells cycle arrest in G1 phase.
Additionally, knockdown of MIAT notably up-regulated the protein level of P16 and down-regulated the protein levels of COX-2 and MMP-9. Conclusion: These observations imply that silencing MIAT inhibits the proliferation, migration and invasion, promotes apoptosis, and induces cell arrest
in G1 phase, partially through up-regulating the expression level of P16 and down-regulating the expression levels of COX-2 and MMP-9, indicating that MIAT may a novel biomarker and therapeutic target for GC.
Publisher
American Scientific Publishers
Subject
Biomedical Engineering,Medicine (miscellaneous),Bioengineering,Biotechnology