Thus, these findings elucidate a novel mechanism by which PPARδ promotes gastric tumorigenesis through interaction with YAP1 and highlights the PPARδ/YAP1/SOX9 axis as a novel therapeutic target in human GC.
In this review, we summarize the recent findings regarding the role of YAP/TAZ in HCC development, and discuss the multifarious mechanisms regulating their activities and their potential contribution to human liver tumorigenesis.
Chromatin immunoprecipitation-sequencing analyses of human YAP1-MAMLD1-positive ependymoma reveal enrichment of NFI and TEAD transcription factor binding site motifs in YAP1-bound regulatory elements, suggesting a role for these transcription factors in YAP1-MAMLD1-driven tumorigenesis.
<b>Conclusions</b>: Our results indicate that YAP1 overexpression is involved in HNSCC tumorigenesis and verteporfin is a potential therapeutic drug for HNSCC.
In conclusion, miR-4319 dampened YAP expression to mitigate the tumorigenesis of NSCLC through inhibiting LIN28-mediated RFX5 stability, which offered an insight into the molecular mechanism underlying miR-4319 in NSCLC development.
Excitingly, our research demonstrates that transfection of mutant plasmid YAP-5SA/S94A or addition of the drug verteporfin, both of which are thought to disrupt the YAP1-TEAD interaction, can arrest the carcinogenesis process.
In this report, we have elucidated a novel role of PR55α-regulated PP2A in the activation of YAP oncoprotein, whose function is required for anchorage-independent growth during oncogenesis of solid tumors.
Here, we provide convincing in vitro and in vivo evidence showing that differential expression and activation of YAP1 oncogene determine individual susceptibility to HPV infection and cervical carcinogenesis.
These findings will provide a significant contribution for targeting the Pin1-YAP/TAZ signaling for the successful treatment of tumorigenesis and drug resistance of breast and other cancers in the future.
Here we show, using an unbiased functional genomic approach, that FUS-DDIT3-expressing mesenchymal stem cells and MLS cell lines are dependent on YAP1, a transcriptional co-activator and central effector of the Hippo pathway involved in tissue growth and tumorigenesis, and that increased YAP1 activity is a hallmark of human MLS Mechanistically, FUS-DDIT3 promotes YAP1 expression, nuclear localization, and transcriptional activity and physically associates with YAP1 in the nucleus of MLS cells.
The major WW domain proteins in the Hippo pathway are YAP and TAZ, which regulate embryonic development, organ growth, tissue regeneration, stem cell pluripotency, and tumorigenesis.
This study offers a molecular framework in which mechanical signals that emerge at the tissue level together with genetic lesions activate YAP/TAZ to induce cell plasticity and tumorigenesis.