Targeting c-MYC by antagonizing PP2A inhibitors in breast cancer
Open accessAbstract
Significance: Increased kinase activity and suppressed phosphatase activity are hallmarks of oncogenic signaling. The transcription factor c-MYC, a master driver of human cancer, is stabilized and activated by persistent serine 62 phosphorylation. The tumor suppressor protein phosphatase 2A (PP2A) targets this site and negatively regulates c-MYC. Here, we show that two cellular inhibitors of PP2A, the SET oncoprotein and cancerous inhibitor of PP2A (CIP2A), are overexpressed in breast cancer, and depletion or inhibition of SET or CIP2A reduces c-MYC expression and activity and decreases the tumorigenic potential of breast cancer cells. These findings strongly suggest that inhibiting SET or CIP2A to reactivate PP2A may be an effective therapeutic strategy for targeting c-MYC in breast cancer.
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CIP2A drives tumour growth in xenograft and transgenic mouse models.
“Of these, CIP2A is widely over-expressed in different human cancer types and drives tumour growth both in xenograft and transgenic mouse models18–24.”
From Structural mechanism for inhibition of PP2A-B56α and oncogenicity by CIP2A (2023) · cites this paper as [22]
In “SET or CIP2A Knockdown Decreases the Tumorigenic Potential of Breast” (page unavailable), the paper reports significantly reduced tumor growth after CIP2A knockdown in breast-cancer xenografts. Our copy does not establish the transgenic-mouse-model part of the claim; its Discussion mentions reduced oncogenic potential after CIP2A deletion but does not identify those models as transgenic. (LLM, conf=0.86)
Experimental — accuracy not yet measuredCIP2A is widely over-expressed in different human cancer types.
“Of these, CIP2A is widely over-expressed in different human cancer types and drives tumour growth both in xenograft and transgenic mouse models18–24.”
From Structural mechanism for inhibition of PP2A-B56α and oncogenicity by CIP2A (2023) · cites this paper as [22]
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References 34 · Cited by 186
- Authors
- Janghorban, M., Farrell, A. S., Allen-Petersen, B. L., Pelz, C., Daniel, C. J., Oddo, J., Langer, E. M., Christensen, D. J., & Sears, R. C.
- Affiliations
- Department of Molecular and Medical Genetics and
- Oregon Health & Science University (US)
- Oncotide Pharmaceuticals (United States) (US)
- Duke University (US)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2014-06-09
- Volume
- 111
- Issue
- 25
- Pages
- 9157-9162
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC4078832
- OpenAlex
- W2053645860
- Cited by
- 186
- References
- 34
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 8 · 2023: 15 · 2022: 17 · 2021: 15 · 2020: 20 · 2019: 23 · 2018: 18 · 2017: 21 · 2016: 16 · 2015: 17 · 2014: 2
- FWCI
- 7.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Defense (BC061306)
- Oregon Health and Science University
- National Cancer Institute (BC061306, CA129040, R01CA129040, R01CA100855, P30CA069533)
- National Institute of General Medical Sciences (T32GM071338)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
- Keywords
- c-Myc, protein phosphatase 2A, breast cancer, CIP2A, PP2A inhibitors, tumor suppressor, apoptosis, post-translational regulation, antitumor strategy
- MeSH terms
- Autoantigens, Breast Neoplasms, DNA-Binding Proteins, Enzyme Inhibitors, Humans, Membrane Proteins, Transcription Factors, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-myc, Drug Delivery Systems, Cell Line, Tumor, Intracellular Signaling Peptides and Proteins, Protein Phosphatase 2, Gene Knockdown Techniques, Histone Chaperones
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