Cited by 360Hippo pathway signaling and YAP/TAZPancreatic and Hepatic Oncology ResearchProtein Kinase Regulation and GTPase Signaling

Downstream of Mutant KRAS, the Transcription Regulator YAP Is Essential for Neoplastic Progression to Pancreatic Ductal Adenocarcinoma

Open access
Zhang, Weiying, Nandakumar, Nivedita, Shi, Yuhao, Manzano, Mark, Smith, Alias, Graham, Garrett, Gupta, Swati, Vietsch, Eveline E. +9 more·2014·Science Signaling

Abstract

Without the transcription regulator YAP, KRAS-mutant pancreatic neoplasia cannot progress into invasive cancer.

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Integrity signals

Registry

Crossref · 10.1126/scisignal.2005049

Cites

126 of 126 references verified0 citation errors · 0 not checkable

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  • YAP1 signaling is essential for initiation of KRAS-driven PDAC.

    “However, previous studies have demonstrated that YAP1 signaling is essential for the initiation of KRAS-driven PDAC.43”

    From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [43]

    The Discussion calls acinar-to-ductal metaplasia (ADM) the initiating step in PDAC development and says Yap is dispensable for it. The Results likewise report that Yap deletion did not affect KRAS-induced ADM. The paper instead finds YAP necessary for subsequent progression to late-stage PanINs and PDAC. (LLM, conf=0.90)

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  • KRAS mutations activate YAP-TAZ and JAK-STAT pathways, leading to release of immunosuppressive cytokines such as CSF-1, IL-4, IL-6.

    “KRAS mutations activate Yes-associated protein-tafazzin (YAP-TAZ) and Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathways, leading to release of immunosuppressive cytokines such as CSF-1, IL-4, IL-6.”

    From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [65]

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Cites

1 retracted

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Research works printed but not linked: 2

  1. [34]Liu T Liu Y Gao H Meng F Yang S Lou G Clinical significance of Yes-associated protein overexpression in cervical carcinoma: The differential effects based on histo-types Int. J. Gynecol. Cancer 2013 23 735 742 23502453
  2. [90]lacobuzio-Donahue CA Ryu B Hruban RH Kern SE Exploring the host desmoplastic response to pancreatic carcinoma: Gene expression of stromal and neoplastic cells at the site of primary invasion Am. J. Pathol 2002 160 91 99 11786403 PMC1867150

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Authors
Zhang, W., Nandakumar, N., Shi, Y., Manzano, M., Smith, A., Graham, G., Gupta, S., Vietsch, E. E., Laughlin, S. Z., Wadhwa, M., Chetram, M., Joshi, M., Wang, F., Kallakury, B., Toretsky, J., Wellstein, A., & Yi, C.
Affiliations
Georgetown University Medical Center (US)
Corresponding author
Yi, Chunling
Venue
Science Signaling
Published
2014-05-06
Volume
7
Issue
324
Pages
ra42-ra42
ISSN
  • 1937-9145 (ISSN-L)
  • 1945-0877
OpenAlex
W2091694499
Cited by
360
References
126
Citations by year
2026: 8 · 2025: 17 · 2024: 18 · 2023: 25 · 2022: 31 · 2021: 42 · 2020: 30 · 2019: 40 · 2018: 32 · 2017: 29 · 2016: 42 · 2015: 34 · 2014: 9
FWCI
19.10
Type
journal article
Language
en
Open access
Locations
  • Science Signaling (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Cancer Institute (R01CA133662, R33CA177466, CA051008, R01CA138212, CA 71508, R01CA071508, P30CA051008, T32CA009686)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
  • Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords
pancreatic ductal adenocarcinoma, KRAS mutation, YAP, Hippo signaling pathway, acinar-to-ductal metaplasia, Trp53, MAPK signaling, tumor microenvironment, secreted factors, cell proliferation, therapeutic target
MeSH terms
YAP-Signaling Proteins, Adenocarcinoma, Animals, Humans, Mutation, Pancreatic Ducts, Phosphoproteins, Genes, ras, RNA, Messenger, Transcription Factors, Genes, p53, Disease Progression, Carcinoma, Pancreatic Ductal, Adaptor Proteins, Signal Transducing, Cell Proliferation, Mice

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