ArticleJournal of experimental & clinical cancer research : CR2018
Inhibiting YAP expression suppresses pancreatic cancer progression by disrupting tumor-stromal interactions.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 70 citations in OpenAlex.
- Fluid shear stress enhances pancreatic cancer motility through YAP activation.Clinical epigenetics · 2026Article
- Pancreatic cancer EMT‑targeted therapy: Molecular mechanisms and clinical translation (Review).International journal of oncology · 2026Review
- The MST4-14-3-3ζ complex promotes pancreatic cancer by activating YAP.Biology direct · 2026Article
- The Hippo signaling pathway modulates pancreatic tissue homeostasis.Cell death discovery · 2025Review
- TEAD-targeting small molecules induce a cofactor switch to regulate the Hippo pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- VCPIP1 facilitates pancreatic adenocarcinoma progression via Hippo/YAP signaling.Cell death & disease · 2025Article
- The role of Hippo/YAP1 in cancer-associated fibroblasts: Literature review and future perspectives.Cancer letters · 2024Review
- Molecular dynamics simulations of a multicellular model with cell-cell interactions and Hippo signaling pathway.PLoS computational biology · 2024Article
- Serum ITIH5 as a novel diagnostic biomarker in cholangiocarcinoma.Cancer science · 2024Article
- Article
- PLVAP protein expression correlated with microbial composition, clinicopathological features, and prognosis of patients with stomach adenocarcinoma.Journal of cancer research and clinical oncology · 2023Article
- Epithelial and stromal co-evolution and complicity in pancreatic cancer.Nature reviews. Cancer · 2023Review
- YAP/TAZ as master regulators in cancer: modulation, function and therapeutic approaches.Nature cancer · 2023Review
- Review
- HNRNPC regulates RhoA to induce DNA damage repair and cancer-associated fibroblast activation causing radiation resistance in pancreatic cancer.Journal of cellular and molecular medicine · 2022Article
- Article
- A Novel Small Molecular Prostaglandin Receptor EP4 Antagonist, L001, Suppresses Pancreatic Cancer Metastasis.Molecules (Basel, Switzerland) · 2022Article
- Extracellular matrix stiffness controls VEGFAngiogenesis · 2022Article
- Harmine suppresses breast cancer cell migration and invasion by regulating TAZ-mediated epithelial-mesenchymal transition.American journal of cancer research · 2022Article
- KRAS as a Key Oncogene in the Clinical Precision Diagnosis and Treatment of Pancreatic Cancer.Journal of Cancer · 2022Review
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14 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHippo/YAP pathway is known to be important for development, growth and organogenesis, and dysregulation of this pathway leads to tumor progression. We and others find that YAP is up-regulated in pancreatic ductal adenocarcinoma (PDAC) and associated with worse prognosis of patients. Activated pancreatic stellate cells (PSCs) forming the components of microenvironment that enhance pancreatic cancer cells (PCs) invasiveness and malignance. However, the role and mechanism of YAP in PDAC tumor-stromal interaction is largely unknown.
methodsThe expression of YAP in Pancreatic cancer cell lines and PDAC samples was examined by Western blot and IHC. The biological role of YAP on cancer cell proliferation, epithelial-mesenchymal transition (EMT) and invasion were evaluated by MTT, Quantitative real-time PCR analysis, Western blot analysis and invasion assay. The effect of YAP on PSC activation was evaluated by PC-PSC co-culture conditions and xenograft PDAC mouse model.
resultsFirstly, knockdown of YAP inhibits PDAC cell proliferation and invasion in vitro. In addition, YAP modulates the PC and PSC interaction via reducing the production of connective tissue growth factor (CTGF) from PCs, inhibits paracrine-mediated PSC activation under PC-PSC co-culture conditions and in turn disrupts TGF-β1-mediated tumor-stromal interactions. Lastly, inhibiting YAP expression prevents tumor growth and suppresses desmoplastic reaction in vivo.
conclusionsThese results demonstrate that YAP contributes to the proliferation and invasion of PC and the activation of PSC via tumor-stromal interactions and that targeting YAP may be a promising therapeutic strategy for PDAC treatment.
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