Implications: Our discovery of a new model supports a distinct paradigm for PPARδ and a crucial oncogenic function of PPARδ in GC through convergence on YAP1/TEAD signaling.
Apart from the classic role of Hippo-YAP1 cascade, in this review, we summarize the current investigations to highlight the prominent role of YAP1/TAZ as a mechanical sensor and responder under mechanical stress and address its potential prognostic and therapeutic value in GC.
Collectively, our findings defined SLC35B4 as an important downstream oncogenic target of YAP1, suggesting that dysregulated signaling of a novel YAP1/SLC35B4 axis promotes GC development and progression, and this axis could be a potential candidate for prognosis and therapeutics in GC.
Collectively, our study demonstrates that the positive feedback loop between LINC01433 and YAP promotes GC progression, and implies that the LINC01433-YAP feedback loop may be a promising therapeutic target for GC treatment.
We reanalyzed human transcriptome data to verify enrichment of YAP signatures in a subpopulation of gastric cancers and found that our model closely reflected the molecular pattern of patients with high YAP activity.
We used the ONCOMINE database and the Kaplan-Meier plotter to analyze YAP1 expression status in different clinicopathological parameters of gastric cancer.
Thus, our study demonstrates that miR-506 may act as a tumor suppressor in GC and that the miR-506/Yap1 axis may help us better understand the molecular mechanisms of GC progression.
This integrative analysis revealed that nine Hippo pathway-related genes, including components [FAT, JUB, LATS2, TEA domain family member 4 (TEAD4) and Yes-associated protein 1 (YAP1)] and targets (CRIM1, CYR61, CTGF and ITGB2), are concurrently hypomethylated at promoter CpG sites and overexpressed in GC tissues.