Increase in CIP2A expression is associated with doxorubicin resistance
Abstract
The cancerous inhibitor of protein phosphatase 2A (CIP2A) increases the migration and metastasis of various cancer cells. Overexpression of CIP2A has been shown to increase the proliferation of MDA-MB-231 cells. We thus assessed whether CIP2A expression is associated with sensitivity to doxorubicin. MDA-MB-231 cells showed an increase in CIP2A expression after treatment with doxorubicin, while MCF-7 cells showed a decrease in CIP2A expression. The overexpression of CIP2A in MCF-7 cells overcame the inhibition of cell proliferation in response to doxorubicin treatment. CIP2A expression was not affected by wild-type or mutant p53. However, mutant p53 blocked doxorubicin-mediated CIP2A down-regulation in HCT116 cells. As a regulation mechanism of doxorubicin-mediated CIP2A expression, we showed that phosphorylated Akt was involved in the suppression of CIP2A expression.
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CIP2A over-expression clinically correlates with relapse from kinase inhibitor therapies.
“CIP2A also broadly regulates cancer cell therapy responses, and its over-expression clinically correlates with relapse from kinase inhibitor therapies27–30.”
From Structural mechanism for inhibition of PP2A-B56α and oncogenicity by CIP2A (2023) · cites this paper as [30]
CIP2A inhibition sensitizes cancer cells to a large number of cancer therapies.
“CIP2A inhibition also sensitizes cancer cells to large number of cancer therapies27,28,30.”
From Structural mechanism for inhibition of PP2A-B56α and oncogenicity by CIP2A (2023) · cites this paper as [30]
CIP2A broadly regulates cancer cell therapy responses.
“CIP2A also broadly regulates cancer cell therapy responses, and its over-expression clinically correlates with relapse from kinase inhibitor therapies27–30.”
From Structural mechanism for inhibition of PP2A-B56α and oncogenicity by CIP2A (2023) · cites this paper as [30]
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- Authors
- Choi, Y. A., Park, J. S., Park, M. Y., Oh, K. S., Lee, M. S., Lim, J.-S., Kim, K. I., Kim, K.-Y., Kwon, J., Yoon, D. Y., Moon, E.-Y., & Yang, Y.
- Affiliations
- Sookmyung Women's University (KR)
- Konkuk University (KR)
- Sejong University (KR)
- Corresponding author
- Yang, Young
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2011-01-15
- Volume
- 585
- Issue
- 5
- Pages
- 755-760
- ISSN
- 0014-5793 (ISSN-L)
- OpenAlex
- W2106755331
- Cited by
- 54
- References
- 27
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 4 · 2022: 1 · 2021: 2 · 2019: 2 · 2018: 6 · 2017: 5 · 2016: 6 · 2015: 7 · 2014: 5 · 2013: 4 · 2012: 9
- FWCI
- 4.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Research Foundation of Korea (NRF) (R11-2005-017-04002-0, 20100028139, 20100026182, R01-2008-000-20127-0)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- CIP2A, doxorubicin resistance, protein phosphatase 2A inhibitor, Akt phosphorylation, p53, breast cancer cells, MDA-MB-231 cells, MCF-7 cells, HCT116 cells, cell proliferation, metastasis, chemoresistance
- MeSH terms
- Autoantigens, Breast Neoplasms, Doxorubicin, Female, Humans, Membrane Proteins, Signal Transduction, Down-Regulation, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Drug Resistance, Neoplasm, HCT116 Cells, Intracellular Signaling Peptides and Proteins, Cell Proliferation, Mutant Proteins, Proto-Oncogene Proteins c-akt
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