98%
921
2 minutes
20
YAP and its paralog TAZ are the nuclear effectors of the Hippo tumour-suppressor pathway, and function as transcriptional co-activators to control gene expression in response to mechanical cues. To identify both common and unique transcriptional targets of YAP and TAZ in gastric cancer cells, we carried out RNA-sequencing analysis of overexpressed YAP or TAZ in the corresponding paralogous gene-knockouts (KOs), TAZ KO or YAP KO, respectively. Gene Ontology (GO) analysis of the YAP/TAZ-transcriptional targets revealed activation of genes involved in platelet biology and lipoprotein particle formation as targets that are common for both YAP and TAZ. However, the GO terms for cell-substrate junction were a unique function of YAP. Further, we found that YAP was indispensable for the gastric cancer cells to re-establish cell-substrate junctions on a rigid surface following prolonged culture on a soft substrate. Collectively, our study not only identifies common and unique transcriptional signatures of YAP and TAZ in gastric cancer cells but also reveals a dominant role for YAP over TAZ in the control of cell-substrate adhesion.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7762230 | PMC |
http://dx.doi.org/10.3390/cancers12123667 | DOI Listing |
Am J Respir Cell Mol Biol
September 2025
Boston University School of Medicine, Department of Biochemistry & Cell Biology, Boston, Massachusetts, United States.
The increased presence of goblet epithelial cells in conducting airways of the respiratory system is common in pulmonary disorders and is often accompanied by disrupted immune and alveolar responses. Signaling effectors that restrict goblet cell production include YAP and TAZ, transcriptional regulators of Hippo signaling, which repress goblet cell differentiation in the airway epithelium. Here, we investigated the acute responses to goblet cell metaplasia that are induced by the conditional loss of YAP/TAZ in club epithelial cells of adult mouse lungs.
View Article and Find Full Text PDFMol Cell
August 2025
Lingang Laboratory, Shanghai 200031, China. Electronic address:
YAP/TAZ are transcriptional co-activators that pair with transcription factor TEA/ATTS domains (TEADs) for modulating the Hippo pathway. Previous works propose the potential role of YAP/TAZ phase separation for transcriptional activation, yet the biomolecular basis of endogenous YAP/TAZ-TEAD condensates remains unclear. Here, we dissect their endogenous morphology, revealing that YAP/TAZ are client proteins recruited to TEAD condensates in various human cell lines.
View Article and Find Full Text PDFMicrobiol Spectr
September 2025
Innovation Center for Cancer Research, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, China.
Chronic hepatitis B virus (HBV) infection is regarded as one of the most serious infectious diseases and a significant global public health concern. Although the neonatal vaccine has been effective in impeding the transmission of HBV, tens of millions of HBV patients are still vulnerable to liver disease and even hepatocellular carcinoma (HCC). In this research, we demonstrated that HBV-encoded circRNA, designated as HBV-circRNA-5, was involved in the tumorigenesis of HCC.
View Article and Find Full Text PDFHippo signaling is a conserved regulator of tissue homeostasis across metazoans. The Ste20 family kinase Hippo/MST activates the NDR family kinase Warts/LATS to inhibit the transcriptional coactivator Yorkie/YAP/TAZ and its transcription factor partner Scalloped/TEAD. In , cell lineages and organ sizes are largely invariant, and classical Hippo phenotypes such as tissue overgrowth are absent.
View Article and Find Full Text PDFJ Am Soc Nephrol
September 2025
Department of Veterans Affairs, Nashville, Tennessee.
Background: In surviving renal proximal tubule cells (RPTCs) following acute kidney injury (AKI), the induction of SOX9 expression plays a crucial role in promoting kidney repair. However, persistent upregulation of SOX9 in RPTCs contributes to the development of chronic kidney disease (CKD). The molecular mechanisms underlying SOX9 induction in response to kidney injury are not completely understood.
View Article and Find Full Text PDF