ArticleOncotarget2016
The GSK3β inhibitor BIS I reverts YAP-dependent EMT signature in PDAC cell lines by decreasing SMADs expression level.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Crosstalk of the Hippo/YAP pathway in the progression of oral potentially malignant disorders to oral squamous cell carcinoma: a systematic review.Frontiers in oral health · 2026Pooled it
- Unraveling the Hippo pathway: YAP/TAZ as central players in cancer metastasis and drug resistance.EXCLI journal · 2025Review
- The investigation of hippo signaling pathway in mouse uterus during peri-implantation period.Archives of gynecology and obstetrics · 2023Article
- Editorial: RNA recognition landscapes and anticancer drug targeting.Frontiers in oncology · 2023Article
- PRDX2 Knockdown Inhibits Extracellular Matrix Synthesis of Chondrocytes by Inhibiting Wnt5a/YAP1/CTGF and Activating IL-6/JAK2/STAT3 Pathways in Deer Antler.International journal of molecular sciences · 2022Article
- NOncogene · 2021Article
- The role of YAP in the control of the metastatic potential of oral cancer.Oncology research · 2021Review
- Biological Significance of YAP/TAZ in Pancreatic Ductal Adenocarcinoma.Frontiers in oncology · 2021Review
- Targeted Disruption of Lats1 and Lats2 in Mice Impairs Adrenal Cortex Development and Alters Adrenocortical Cell Fate.Endocrinology · 2020Article
- Yes-associated protein (YAP) predicts poor prognosis and regulates progression of esophageal squamous cell cancer through epithelial-mesenchymal transition.Experimental and therapeutic medicine · 2019Article
- Review
- Differential YAP nuclear signaling in healthy and dystrophic skeletal muscle.American journal of physiology. Cell physiology · 2019Article
- EMT induced by loss of LKB1 promotes migration and invasion of liver cancer cells through ZEB1-induced YAP signaling.Oncology letters · 2018Article
- DNA binding partners of YAP/TAZ.BMB reports · 2018Review
- The roles of ING5 expression in ovarian carcinogenesis and subsequent progression: a target of gene therapy.Oncotarget · 2017Article
- Yes-associated protein and immunosuppressive microenvironment in pancreatic cancer development: a new strategy to improve immunotherapy efficacy?Journal of thoracic disease · 2017Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Yes-associated protein, YAP, is a transcriptional co-activator, mediating the Epithelial to Mesenchymal Transition program in pancreatic ductal adenocarcinoma (PDAC). With the aim to identify compounds that can specifically modulate YAP functionality in PDAC cell lines, we performed a small scale, drug-based screening experiment using YAP cell localization as the read-out. We identified erlotinib as an inducer of YAP cytoplasmic localization, an inhibitor of the TEA luciferase reporter system and the expression of the bona fide YAP target gene, Connective Tissue Growth Factor CTGF. On the other hand, BIS I, an inhibitor of PKCδ and GSK3β, caused YAP accumulation into the nucleus. Activation of β-catenin reporter and interfering experiments show that inhibition of the PKCδ/GSK3β pathway triggers YAP nuclear accumulation inducing YAP/TEAD transcriptional response. Inhibition of GSK3β by BIS I reduced the expression levels of SMADs protein and reduced YAP contribution to EMT. Notably, BIS I reduced proliferation, migration and clonogenicity of PDAC cells in vitro, phenocopying YAP genetic down-regulation. As shown by chromatin immunoprecipitation experiments and YAP over-expressing rescue experiments, BIS I reverted YAP-dependent EMT program by modulating the expression of the YAP target genes E-cadherin, vimentin, CTGF and of the newly identified target, CD133. In conclusion, we identified two different molecules, erlotinib and BIS I, modulating YAP functionality although via different mechanisms of action, with the second one specifically inhibiting the YAP-dependent EMT program in PDAC cell lines.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.