A p53 Super-tumor Suppressor Reveals a Tumor Suppressive p53-Ptpn14-Yap Axis in Pancreatic Cancer
Open accessAbstract
The p53 transcription factor is a critical barrier to pancreatic cancer progression. To unravel mechanisms of p53-mediated tumor suppression, which have remained elusive, we analyzed pancreatic cancer development in mice expressing p53 transcriptional activation domain (TAD) mutants. Surprisingly, the p53 53,54 TAD2 mutant behaves as a "super-tumor suppressor," with an enhanced capacity to both suppress pancreatic cancer and transactivate select p53 target genes, including Ptpn14. Ptpn14 encodes a negative regulator of the Yap oncoprotein and is necessary and sufficient for pancreatic cancer suppression, like p53. We show that p53 deficiency promotes Yap signaling and that PTPN14 and TP53 mutations are mutually exclusive in human cancers. These studies uncover a p53-Ptpn14-Yap pathway that is integral to p53-mediated tumor suppression.
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Introducing wild-type TP53 into cancer cells could alter sensitivity to treatments.
“Introducing wild-type TP53 into cancer cells could alter sensitivity to treatments [18].”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [18]
The Results section, “The p53-Ptpn14-Yap axis is altered in human cancers” (page unavailable), reports that verteporfin inhibits growth in p53-deficient human cancer cells but not p53-proficient counterparts. This supports a link between p53 status and sensitivity to a treatment, but the cited passage does not show that introducing wild-type TP53 into cancer cells changes their sensitivity. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe p53-Ptpn14-Yap axis is a critical pathway in pancreatic cancer suppression, offering potential therapeutic avenues.
“The p53-Ptpn14-Yap axis emerges as a critical pathway in pancreatic cancer suppression, offering potential therapeutic avenues [18].”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [18]
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Cites
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p53 mutant mice that display early ageing-associated phenotypes
Tyner, S. D., Venkatachalam, S., Choi, J., Jones, S., Ghebranious, N., Igelmann, H., Lu, X., Soron, G., Cooper, B., Brayton, C., et al. (2002) · Nature · doi:10.1038/415045a · Cited by 1,459 · cited 2× · see citing works
“Mice expressing either of two N-terminal deletion variants (p53 or p53) display premature aging, which is at least in part attributable to effects on gene expression (Maier et al., 2004; Tyner et al., 2002).”
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“Studies using genetically engineered mouse models have demonstrated that Kras activation along with mutation of one copy of any of these tumor suppressor genes is sufficient to drive PDAC development (Aguirre et al., 2003; Bardeesy et al., 2006a, 2006b; Hingorani et al., 2005; Izeradjene et al., 2007).”
The role of the transcriptional regulator Ptf1a in converting intestinal to pancreatic progenitors
Kawaguchi, Y., Cooper, B., Gannon, M., Ray, M., MacDonald, R. J., & Wright, C. V. E. (2002) · Nature Genetics · doi:10.1038/ng959 · Cited by 1,007 · cited 1× · see citing works
“Kras+/LSL-G12D;Ptf1a-Cre;Trp53+/+ and Kras+/LSL-G12D;Ptf1a-Cre;Trp53fl/fl mice were used for the Yap localization analysis (Jonkers et al., 2001; Kawaguchi et al., 2002).”
Yap1 Activation Enables Bypass of Oncogenic Kras Addiction in Pancreatic Cancer
Kapoor, A., Yao, W., Ying, H., Hua, S., Liewen, A., Wang, Q., Zhong, Y., Wu, C.-J., Sadanandam, A., Hu, B., et al. (2014) · Cell · doi:10.1016/j.cell.2014.06.003 · Cited by 716 · cited 4× · see citing works
“Recent studies continue to illuminate the contribution of new proteins to PDACdevelopment, such as the Yap transcriptional coactivator, which is essential for progression of preneoplastic lesions to PDAC in mouse models and can even substitute for Kras activation (Kapoor et al., 2014; Zhang et al., 2014).”
InfluentialCharacterization of Hippo Pathway Components by Gene Inactivation
Plouffe, S. W., Meng, Z., Lin, K. C., Lin, B., Hong, A. W., Chun, J. V., & Guan, K.-L. (2016) · Molecular Cell · doi:10.1016/j.molcel.2016.10.034 · Cited by 275 · see citing works
PTPN14 is required for the density-dependent control of YAP1
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Self-citationEpithelial and stromal co-evolution and complicity in pancreatic cancer
Hingorani, S. R. (2023) · Nature Reviews Cancer · doi:10.1038/s41568-022-00530-w · Cited by 108 · see citing works
Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer
Stefanoudakis, D., Frountzas, M., Schizas, D., Michalopoulos, N. V., Drakaki, A., & Toutouzas, K. G. (2024) · Current Issues in Molecular Biology · doi:10.3390/cimb46040177 · Cited by 110 · see citing works
Multifaceted role for p53 in pancreatic cancer suppression
Mello, S. S., Flowers, B. M., Mazur, P. K., Lee, J. J., Müller, F., Denny, S. K., Ferreira, S., Hanson, K., Kim, S. K., Greenleaf, W. J., et al. (2023) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2211937120 · Cited by 55 · see citing works
Self-citation
- Authors
- Mello, S. S., Valente, L. J., Raj, N., Seoane, J. A., Flowers, B. M., McClendon, J., Bieging-Rolett, K. T., Lee, J., Ivanochko, D., Kozak, M. M., Chang, D. T., Longacre, T. A., Koong, A. C., Arrowsmith, C. H., Kim, S. K., Vogel, H., Wood, L. D., Hruban, R. H., Curtis, C., & Attardi, L. D.
- Affiliations
- Stanford Medicine (US)
- University of Toronto (CA)
- Johns Hopkins University (US)
- Corresponding author
- Attardi, Laura D.
- ORCID
- Mello, Stephano S.
- Valente, Liz J.
- Raj, Nitin
- Flowers, Brittany M.
- McClendon, Jacob
- Bieging-Rolett, Kathryn T.
- Ivanochko, Danton
- Kozak, Margaret M.
- Chang, Daniel T.
- Longacre, Teri A.
- Koong, Albert C.
- Arrowsmith, Cheryl H.
- Kim, Seung K.
- Vogel, Hannes
- Wood, Laura D.
- Hruban, Ralph H.
- Curtis, Christina
- Attardi, Laura D.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 32
- Issue
- 4
- Pages
- 460-473.e6
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC5659188
- OpenAlex
- W2761908907
- Cited by
- 179
- References
- 11
- Citations by year
- 2026: 8 · 2025: 16 · 2024: 13 · 2023: 21 · 2022: 20 · 2021: 33 · 2020: 28 · 2019: 18 · 2018: 15 · 2017: 5
- FWCI
- 7.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Canadian Natural Sciences and Engineering Research Council
- NIH (R21 CA169673, R01 CA140875, R35 CA197591, DK10261201, CA21192701)
- Susan G. Komen Postdoctoral Fellowship (PDF16377256)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Keywords
- p53, PTPN14, YAP, pancreatic cancer, tumor suppression, YAP signaling, p53 target genes, TP53 mutation, mutual exclusivity, mouse model
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Humans, Mutation, Nuclear Proteins, Pancreatic Neoplasms, Transcription Factors, Signal Transduction, Tumor Suppressor Protein p53, Cell Cycle Proteins, Gene Expression Profiling, Cell Proliferation, Mice, Protein Tyrosine Phosphatases, Non-Receptor
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