LINC00662 promotes gastric cancer cell growth by modulating the Hippo-YAP1 pathway

Long non-coding RNAs (lncRNAs) function as vital regulators of the progression of various diseases, particularly cancers. In the present study, utilizing the Cancer Genome Atlas (TCGA) data set and a series of cell experiments and clinical tissue samples assays, we found that LINC00662 expression wa...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Biochemical and biophysical research communications 2018-11, Vol.505 (3), p.843-849
Hauptverfasser: Liu, Zhen, Yao, Yangyang, Huang, Shanshan, Li, Li, Jiang, Bailing, Guo, Hui, Lei, Wan, Xiong, Jianping, Deng, Jun
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Long non-coding RNAs (lncRNAs) function as vital regulators of the progression of various diseases, particularly cancers. In the present study, utilizing the Cancer Genome Atlas (TCGA) data set and a series of cell experiments and clinical tissue samples assays, we found that LINC00662 expression was significantly up-regulated in gastric cancer (GC) tissues and cell lines. High expression of LINC00662 predicted poor prognosis compared to in patients showing low expression. Knockdown of LINC00662 expression decreased GC cell proliferation and increased the chemo-sensitivity of GC cells. Further, we demonstrated that knockdown of LINC00662 suppressed the Hippo-YAP1 signaling pathway in GC cells. Mechanistically, LINC00662 regulated YAP1-mediated GC cell proliferation by sponging miR-497-5p. Overall, our results revealed a critical role for the LINC00662-miR-497-5p–YAP1 axis in GC cell growth, providing a new target for GC. •High expression of LINC00662 predicted poor prognosis of gastric cancer patients.•LINC00662 activated Hippo-YAP1 pathway via sponging miR-497-5p.•The LINC00662-miR-497-5p-YAP1 signal axis may be a target of gastric cancer.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2018.09.191