Cited by 196Protein Kinase Regulation and GTPase SignalingWnt/β-catenin signaling in development and cancerPancreatic and Hepatic Oncology Research

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K-Ras Promotes Tumorigenicity through Suppression of Non-canonical Wnt Signaling

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Wang, Man-Tzu, Holderfield, Matthew, Galeas, Jacqueline, Delrosario, Reyno, To, Minh D., Balmain, Allan, McCormick, Frank·2015·Cell

DOI 10.1016/j.cell.2015.10.041

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Abstract

K-Ras and H-Ras share identical effectors and have similar properties; however, the high degree of tumor-type specificity associated with K-Ras and H-Ras mutations suggests that they have unique roles in oncogenesis. Here, we report that oncogenic K-Ras, but not H-Ras, suppresses non-canonical Wnt/Ca(2+) signaling, an effect that contributes strongly to its tumorigenic properties. K-Ras does this by binding to calmodulin and so reducing CaMKii activity and expression of Fzd8. Restoring Fzd8 in K-Ras mutant pancreatic cells suppresses malignancy, whereas depletion of Fzd8 in H-Ras(V12)-transformed cells enhances their tumor initiating capacity. Interrupting K-Ras-calmodulin binding using genetic means or by treatment with an orally active protein kinase C (PKC)-activator, prostratin, represses tumorigenesis in K-Ras mutant pancreatic cancer cells. These findings provide an alternative way to selectively target this "undruggable" protein.

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Authors: Wang, M.-T., Holderfield, M., Galeas, J., Delrosario, R., To, M. D., Balmain, A., & McCormick, F.
Affiliations: University of California, San Francisco (US)
Corresponding author: McCormick, Frank
ORCID: Holderfield, Matthew
Galeas, Jacqueline
Delrosario, Reyno
To, Minh D.
Balmain, Allan
McCormick, Frank
Venue: Cell
Publisher: Elsevier BV
Published: 2015-11
Volume: 163
Issue: 5
Pages: 1237-1251
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2015.10.041
OpenAlex: W2175955272
Cited by: 196
References: 64
Citations by year: 2026: 13 · 2025: 4 · 2024: 6 · 2023: 14 · 2022: 18 · 2021: 19 · 2020: 23 · 2019: 17 · 2018: 21 · 2017: 30 · 2016: 27 · 2015: 1
FWCI: 11.44
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 384 d)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Funders: Lustgarten Foundation
Daiichi-Sankyo
National Institutes of Health
Daiichi Sankyo Europe
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
Keywords: KRAS, H-Ras, calmodulin, CaMKII, FZD8, pancreatic cancer, tumorigenicity, prostratin, protein kinase C, tumor initiation
MeSH terms: Amino Acid Sequence, Animals, Calmodulin, Disease Models, Animal, Female, Humans, Molecular Sequence Data, Pancreatic Neoplasms, Papilloma, Phorbol Esters, Phosphorylation, Protein Binding, Genes, ras, Receptors, Cell Surface, Proto-Oncogene Proteins p21(ras), Animals, Genetically Modified, Cell Line, Tumor, Mice, Wnt Signaling Pathway

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K-Ras Promotes Tumorigenicity through Suppression of Non-canonical Wnt Signaling

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