Logo image
Therapeutic relevance of the protein phosphatase 2A in cancer
Journal article   Open access   Peer reviewed

Therapeutic relevance of the protein phosphatase 2A in cancer

Chelsea E Cunningham, Shuangshuang Li, Frederick S Vizeacoumar, Kalpana Kalyanasundaram Bhanumathy, Joo Sang Lee, Sreejit Parameswaran, Levi Furber, Omar Abuhussein, James M Paul, Megan McDonald, …
Oncotarget, Vol.7(38), pp.61544-61561
09/20/2016
DOI: 10.18632/oncotarget.11399
PMCID: PMC5308671
PMID: 27557495
url
https://doi.org/10.18632/oncotarget.11399View
Published (Version of record) Open Access

Abstract

Chromosomal Instability (CIN) is regarded as a unifying feature of heterogeneous tumor populations, driving intratumoral heterogeneity. Polo-Like Kinase 1 (PLK1), a serine-threonine kinase that is often overexpressed across multiple tumor types, is one of the key regulators of CIN and is considered as a potential therapeutic target. However, targeting PLK1 has remained a challenge due to the off-target effects caused by the inhibition of other members of the polo-like family. Here we use synthetic dosage lethality (SDL), where the overexpression of PLK1 is lethal only when another, normally non-lethal, mutation or deletion is present. Rather than directly inhibiting PLK1, we found that inhibition of PP2A causes selective lethality to PLK1-overexpressing breast, pancreatic, ovarian, glioblastoma, and prostate cancer cells. As PP2A is widely regarded as a tumor suppressor, we resorted to gene expression datasets from cancer patients to functionally dissect its therapeutic relevance. We identified two major classes of PP2A subunits that negatively correlated with each other. Interestingly, most mitotic regulators, including PLK1, exhibited SDL interactions with only one class of PP2A subunits (PPP2R1A, PPP2R2D, PPP2R3B, PPP2R5B and PPP2R5D). Validation studies and other functional cell-based assays showed that inhibition of PPP2R5D affects both levels of phospho-Rb as well as sister chromatid cohesion in PLK1-overexpressing cells. Finally, analysis of clinical data revealed that patients with high expression of mitotic regulators and low expression of Class I subunits of PP2A improved survival. Overall, these observations point to a context-dependent role of PP2A that warrants further exploration for therapeutic benefits.
Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Apoptosis - drug effects Cantharidin - pharmacology Cantharidin - therapeutic use Cell Cycle Proteins - antagonists & inhibitors Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Chromosomal Instability - drug effects Enzyme Inhibitors - pharmacology Enzyme Inhibitors - therapeutic use Gene Knockdown Techniques Genes, Tumor Suppressor - drug effects HCT116 Cells Humans Mitosis - drug effects Mutation Neoplasms - drug therapy Neoplasms - genetics Neoplasms - pathology Phosphorylation Protein Phosphatase 2 - antagonists & inhibitors Protein Phosphatase 2 - genetics Protein Phosphatase 2 - metabolism Protein-Serine-Threonine Kinases - antagonists & inhibitors Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Proto-Oncogene Proteins - antagonists & inhibitors Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Retinoblastoma Binding Proteins - metabolism RNA Interference RNA, Small Interfering - metabolism Ubiquitin-Protein Ligases - metabolism

Details

Metrics

Logo image