LATS1 (Large Tumor Suppressor Kinase 1)

Protein phosphatase 4 catalytic subunit (PPP4C) was found to interact with MST4 and reduce its function, thus promoting growth and immunosuppression in NSCLC by activating YAP1. This study demonstrates that PPP4C-mediated MST4 degradation contributes to growth activity and immunosuppression in NSCLC by restoring YAP1 activity, suggesting PPP4C and MST4 as potential targets for NSCLC management.

SS restrains cervical cancer progression by inducing apoptosis and accelerating autophagosome turnover through activation of the YAP-Hippo axis. These findings highlight SS and YAP-directed modulation in general, as promising avenues for future cervical cancer therapy development.

At the signaling level, CCT5 knockdown enhanced phosphorylation of MST1, LATS1, and YAP, without significant changes in total protein levels, suggesting activation of Hippo/YAP signaling. These findings highlight CCT5 as an oncogenic factor in bladder cancer, potentially acting through the regulation of Hippo/YAP signaling, and propose its potential as a biomarker and therapeutic target in bladder cancer.

It explores the crosstalk between Hippo-YAP/TAZ signalling and other oncogenic pathways, including Wnt/β-catenin and PI3K/Akt, as well as the influence of tumour microenvironmental factors such as hypoxia and extracellular matrix stiffness on pathway activation. Additionally, emerging therapeutic strategies targeting YAP/TAZ-TEAD interactions and upstream regulators are discussed, offering potential avenues for improving gastric cancer outcomes in diagnosis and treatment.

Our findings are further supported by in-silico analysis that showed strong binding affinity of TAP with key regulatory genes. Collectively, these findings suggest that TAP is a hepatotoxic agent and warrant further clinical trials to evaluate its effects in humans.

Quercetin inhibits proliferation and migration and promotes apoptosis of gastric cancer cells by promoting phosphorylation-mediated inactivation of YAP.

Mechanistically, LATS1 associated with TBK1 upon cytosolic nucleic acid stimulation and promoted TBK1 signaling and activation in a kinase dependent manner. Altogether, our findings reveal that cytosolic nucleic acid sensing pathways elicit Hippo/LATS1 activation to govern TBK1 signaling events to result in IFN-I activation.

Our results suggest that the potential phosphorylation sites are Ser 167 and Thr 170, distinct from the Thr 12 and Thr 35 in human MOB1. Computational protein-protein interaction studies confirm the plausibility of the identified phosphorylation sites.

soja proteins and peptides inhibited inflammation by decreasing pro-inflammatory cytokines IL-6, IL-1β, and MCP-1, phosphorylating YAP1 and LATS1/2, and increasing YAP1 cytoplasmic retention, thus activating the Hippo pathway. The results suggest that soybean proteins and peptides inhibited inflammation through the Hippo pathway, offering novel developments of functional food ingredients or supplements for a healthier diet.

In conclusion, GA activates the Hippo pathway and promotes YAP1 translocation to the cytoplasm, leading to its degradation and subsequent inhibition of PSC activation and fibrosis. These findings highlight the critical role of ubiquitin-mediated YAP1 degradation in regulating PSC activity and offer novel insights into the therapeutic potential of GA for treating pancreatic fibrosis.

GCs protect against HIRI by activating the EPAC2-Rap1-Hippo-YAP-JNK axis to promote autophagy and suppress apoptosis. These findings provide mechanistic insight into the hepatoprotective actions of GCs and support their evidence-based ethnopharmacological use as a promising therapeutic approach for ischemic liver injury.

These findings revealed a previously undefined mechanism of action of GSK690693 as a Hippo pathway inhibitor, underscoring its efficacy in mitigating ER-positive breast cancer progression. Given the broader implications of Hippo pathway dysregulation in multiple cancers, GSK690693 could be part of a combination regimen for various malignancies.