Evaluation of PPP2R2A as a prostate cancer susceptibility gene: A comprehensive germline and somatic study
Open accessAbstract
PPP2R2A, mapped to 8p21.2, codes for the α isoform of the regulatory B55 subfamily of protein phosphatase 2 (PP2A). PP2A is one of the four major serine/threonine phosphatases and is implicated in the negative control of cell growth and division. Because of its known functions and location within a chromosomal region where evidence for linkage and somatic loss of heterozygosity was found, we hypothesized that either somatic copy number changes or germline sequence variants in PPP2R2A may increase prostate cancer (PCa) risk. We examined PPP2R2A deletion status in 141 PCa samples using Affymetrix SNP arrays. It was found that PPP2R2A was commonly (67.1%) deleted in tumor samples, including a homozygous deletion in three tumors (2.1%). We performed a mutation screen for PPP2R2A in 96 probands of hereditary prostate cancer families. No high risk mutations were identified. In addition, we re-analyzed 10 SNPs of PPP2R2A in sporadic PCa cases and controls. No significant differences in the allele and genotype frequencies were observed among either PCa cases and controls or PCa aggressive and non-aggressive cases. Taken together, these results suggest that a somatic deletion rather than germline sequence variants of PPP2R2A may play a more important role in PCa susceptibility.
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Deletions affecting PPP2R2A have been observed in prostate, ovarian and breast epithelial tumors.
“Deletions affecting the PPP2R2A gene have been observed in a number of epithelial tumors in prostate, ovarian and breast cancer patients (Cheng et al., 2011; Watt et al., 2017; Youn and Simon, 2013).”
From PP2A holoenzymes, substrate specificity driving cellular functions and deregulation in cancer (2019) · cites this paper as Cheng et al., 2011
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The Greatwall/PP2A-B55α axis remodels the G2/M boundary and shapes cellular dependence on PKMYT1Preprint
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- Authors
- Cheng, Y., Liu, W., Kim, S.-T., Sun, J., Lu, L., Sun, J., Zheng, S. L., Isaacs, W. B., & Xu, J.
- Affiliations
- Wake Forest University Health Sciences (US)
- Johns Hopkins Medicine (US)
- Corresponding author
- Isaacs, William B.
- Xu, Jianfeng
- Venue
- Cancer Genetics
- Publisher
- Elsevier BV
- Published
- 2011-07
- Volume
- 204
- Issue
- 7
- Pages
- 375-381
- ISSN
- 2210-7762 (ISSN-L)
- PMC
- PMC3722858
- OpenAlex
- W2164348209
- Cited by
- 64
- References
- 32
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 4 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 2 · 2019: 8 · 2018: 6 · 2017: 5 · 2016: 3 · 2015: 6 · 2014: 4 · 2013: 4 · 2012: 2
- FWCI
- 2.73
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Genetics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (CA95052, R01CA095052)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- PPP2R2A, prostate cancer, susceptibility genes, protein phosphatase 2A, somatic deletions, germline mutations, copy number loss, hereditary prostate cancer, single nucleotide polymorphisms, tumor aggressiveness
- MeSH terms
- Alleles, DNA Mutational Analysis, DNA, Neoplasm, Exons, Gene Frequency, Humans, Genetic Linkage, Male, Middle Aged, Prostatic Neoplasms, Gene Deletion, Germ-Line Mutation, Genetic Predisposition to Disease, 5' Untranslated Regions, 3' Untranslated Regions, Polymorphism, Single Nucleotide, Protein Phosphatase 2, DNA Copy Number Variations
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