The DOI matches its Crossref record; 45 of the 47 references it cites were found in a registry or an index.
Yes-Associated Protein Up-regulates Jagged-1 and Activates the NOTCH Pathway in Human Hepatocellular Carcinoma
Open accessAbstract
Background & aims Cancer cells often lose contact inhibition to undergo anchorage-independent proliferation and become resistant to apoptosis by inactivating the Hippo signaling pathway, resulting in activation of the transcriptional co-activator yes-associated protein (YAP). However, the oncogenic mechanisms of YAP activity are unclear.Methods By using cross-species analysis of expression data, the Notch ligand Jagged-1 (Jag-1) was identified as a downstream target of YAP in hepatocytes and hepatocellular carcinoma (HCC) cells. We analyzed the functions of YAP in HCC cells via overexpression and RNA silencing experiments. We used transgenic mice that overexpressed a constitutively activated form of YAP (YAP(S127A)), and measured protein levels in HCC, colorectal and pancreatic tumor samples from patients.Results Human HCC cell lines and mouse hepatocytes that overexpress YAP(S127A) up-regulated Jag-1, leading to activation of the Notch pathway and increased proliferation. Induction of Jag-1, activation of Notch, and cell proliferation required binding of YAP to its transcriptional partner TEA domain family member 4 (TEAD4); TEAD4 binding required the Mst1/2 but not β-catenin signaling. Levels of YAP correlated with Jag-1 expression and Notch signaling in human tumor samples and correlated with shorter survival times of patients with HCC or colorectal cancer.Conclusions The transcriptional regulator YAP up-regulates Jag-1 to activate Notch signaling in HCC cells and mouse hepatocytes. YAP-dependent activity of Jag-1 and Notch correlate in human HCC and colorectal tumor samples with patient survival times, suggesting the use of YAP and Notch inhibitors as therapeutics for gastrointestinal cancer. Transcript profiling: microarray information was deposited at the Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?token=jxepvsumwosqkve&acc=GSE35004).
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In the citing paper
“Despite the protective effects of IL-6, YAP-mediated Notch signaling activation contributed to tumor growth in human hepatocellular carcinoma and murine hepatocytes (Tschaharganeh et al., 2013”
From Targeting Interleukin-6 Signaling in Clinic (2019) · cites this paper as Tschaharganeh et al., 2013
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“Over the years, a number of inhibitors targeting YAP/TAZ-TEAD have been reported, including peptides such as super-TDU (173),437 and small molecules such as verteporfin (174) and MGH-CP1 (175).438–440”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [439]
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Cites
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Self-citationExpression of Yes-associated protein in common solid tumors
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Self-citationYes‐associated protein is an independent prognostic marker in hepatocellular carcinoma
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Notch Signaling Is Activated in Human Hepatocellular Carcinoma and Induces Tumor Formation in Mice
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“Thus, YAP-dependent activation of the Jag-1/Notch pathway in these mice is probably relevant for the formation of HCC.5,8,32,35 YAP regulates target gene transcription in tumor and non-malignantly transformed cells through interaction with different transcription factors including TEAD family members.18 Our results de…”
Using TESS to Predict Transcription Factor Binding Sites in DNA Sequence
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“Although transcription factors are believed to be non- 21 druggable due to large and stable protein/DNA surface interactions, crystal structure analysis of the YAP/TEAD4 complex demonstrated that the proteins are connected mainly via two short helices, one in the C-terminal domain of TEAD4 and one in the N-terminal re…”
InfluentialQi, R., An, H., Yu, Y., Zhang, M., Liu, S., Xu, H., Guo, Z., Cheng, T., & Cao, X. (2003) · PubMed · Cited by 241
Notch signaling inhibits hepatocellular carcinoma following inactivation of the RB pathway
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“The Hippo/YAP axis may also regulate the activity of additional pathways, including Sonic hedgehog (Shh)(27) as well as FGF, BDNF, and CTGF signaling.(3,28) As has been demonstrated for other cellular pathways, intensive cross talk argues for a contextdependent behavior of Hippo/YAP under physiological and pathophysio…”
Constitutive Notch2 signaling induces hepatic tumors in mice
Dill, M. T., Tornillo, L., Fritzius, T., Terracciano, L., Semela, D., Bettler, B., Heim, M. H., & Tchorz, J. S. (2012) · Hepatology · doi:10.1002/hep.26165 · Cited by 115 · cited 3×
“Thus, YAP-dependent activation of the Jag-1/Notch pathway in these mice is probably relevant for the formation of HCC.5,8,32,35 YAP regulates target gene transcription in tumor and non-malignantly transformed cells through interaction with different transcription factors including TEAD family members.18 Our results de…”
YAP: At the crossroad between transformation and tumor suppression
Bertini, E., Oka, T., Sudol, M., Strano, S., & Blandino, G. (2009) · Cell Cycle · doi:10.4161/cc.8.1.7259 · Cited by 112 · cited 1×
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Self-citationOverexpression of Far Upstream Element Binding Proteins
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Self-citationNotch1‐Snail1‐E‐cadherin pathway in metastatic hepatocellular carcinoma
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IKKα Activation of NOTCH Links Tumorigenesis via FOXA2 Suppression
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Glycoprotein 130–dependent pathways in host hepatocytes are important for liver repopulation in mice
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Metadata
- Authors
- Tschaharganeh, D. F., Chen, X., Latzko, P., Malz, M., Gaida, M. M., Felix, K., Ladu, S., Singer, S., Pinna, F., Gretz, N., Sticht, C., Tomasi, M. L., Delogu, S., Evert, M., Fan, B., Ribback, S., Jiang, L., Brozzetti, S., Bergmann, F., Dombrowski, F., Schirmacher, P., Calvisi, D. F., & Breuhahn, K.
- Affiliations
- University Hospital Heidelberg (DE)
- University of California, San Francisco (US)
- University of Chieti-Pescara (IT)
- Medizinische Fakultät Mannheim (DE)
- University of Southern California (US)
- Universität Greifswald (DE)
- Sapienza University of Rome (IT)
- Corresponding author
- Breuhahn, Kai
- ORCID
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2013-06
- Volume
- 144
- Issue
- 7
- Pages
- 1530-1542.e12
- ISSN
- 0016-5085 (ISSN-L)
- PMC
- PMC3665638
- OpenAlex
- W2060323466
- Cited by
- 326
- References
- 47
- Citations by year
- 2026: 8 · 2025: 16 · 2024: 16 · 2023: 19 · 2022: 26 · 2021: 29 · 2020: 35 · 2019: 26 · 2018: 26 · 2017: 25 · 2016: 28 · 2015: 35 · 2014: 28 · 2013: 8
- FWCI
- 19.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- YAP, Jagged1, Notch signaling, hepatocellular carcinoma, TEAD4, MST1/2, Hippo signaling pathway, colorectal cancer, pancreatic cancer, cell proliferation, patient survival, transcriptional coactivator, therapeutic target
- MeSH terms
- Serrate-Jagged Proteins, Jagged-1 Protein, YAP-Signaling Proteins, TEA Domain Transcription Factors, Animals, Calcium-Binding Proteins, DNA-Binding Proteins, Carcinoma, Hepatocellular, Humans, Liver Neoplasms, Membrane Proteins, Muscle Proteins, Phosphoproteins, Transcription Factors, Up-Regulation, Gene Expression Regulation, Neoplastic, Cell Cycle Proteins, Hepatocytes, Intercellular Signaling Peptides and Proteins, Cell Line, Tumor, Adaptor Proteins, Signal Transducing, Cell Proliferation, Mice, Receptors, Notch
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