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CREB up-regulates long non-coding RNA, HULC expression through interaction with microRNA-372 in liver cancer
The study elucidates that fine tuning of HULC expression is part of an auto-regulatory loop in which it’s inhibitory to expression and activity of miR-372 allows lncRNA up-regulated expression in liver cancer.
circRNA_104075 stimulates YAP-dependent tumorigenesis through the regulation of HNF4a and may serve as a diagnostic marker in hepatocellular carcinoma
It is determined that circ_104075 was highly expressed in HCC and its upstream and downstream regulatory mechanisms are elucidated and it has the potential to serve as a new diagnostic biomarker in H CC.
Sox9, a key transcription factor of bone morphogenetic protein‐2‐induced chondrogenesis, is activated through BMP pathway and a CCAAT box in the proximal promoter
Insight is provided into the mechanisms underlying B MP‐2‐regulated Sox9 expression and activity in MEFs, and differential roles of BMP‐2/p38 and BMP•2/Smad pathways in modulating the function of Sox9 during chondrogenesis are suggested.
NRAGE promotes cell proliferation by stabilizing PCNA in a ubiquitin-proteasome pathway in esophageal carcinomas.
This study highlights a unique role of NRAGE and implies that NRAGE is likely to be an attractive oncotarget in developing novel genetic anticancer therapeutic strategies for esophageal squamous cell carcinomas.
The essential role of YAP O-GlcNAcylation in high-glucose-stimulated liver tumorigenesis
It is found via in vitro cell-based and in vivo mouse model experiments that O-GlcNAcylation of YAP was required for high-glucose-induced liver tumorigenesis and is a potential therapeutic intervention point for treating liver cancer associated with high blood glucose levels and possibly diabetes.
Mutual interaction between YAP and CREB promotes tumorigenesis in liver cancer
It is found that YAP‐CREB interaction is critical for liver cancer cell survival and maintenance of transformative phenotypes, both in vitro and in vivo, and there is a novel positive autoregulatory feedback loop underlying the interaction between YAP and CREB.
Mutual interaction between YAP and c-Myc is critical for carcinogenesis in liver cancer.
Cluster of Differentiation 166 (CD166) Regulated by Phosphatidylinositide 3-Kinase (PI3K)/AKT Signaling to Exert Its Anti-apoptotic Role via Yes-associated Protein (YAP) in Liver Cancer*
It is reported that gene silencing of CD166 promoted apoptosis via down-regulation of Bcl-2 in liver cancer cells, indicating that CD166 is regulated by PI3K/AKT to exert its anti-apoptotic role via YAP.