ArticleMolecular cancer therapeutics2011
Modulation of protein phosphatase 2A activity alters androgen-independent growth of prostate cancer cells: therapeutic implications.
Article in Molecular cancer therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 62 citations in OpenAlex.
- Paclitaxel hyperthermia suppresses gastric cancer migration through MiR-183-5p/PPP2CA/AKT/GSK3β/β-catenin axis.Journal of cancer research and clinical oncology · 2024Article
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- Reciprocal regulation of CIP2A and AR expression in prostate cancer cells.Discover oncology · 2022Article
- MYB interacts with androgen receptor, sustains its ligand-independent activation and promotes castration resistance in prostate cancer.British journal of cancer · 2022Article
- PP2A promotes apoptosis and facilitates docetaxel sensitivity via the PP2A/p-eIF4B/XIAP signaling pathway in prostate cancer.Oncology letters · 2022Article
- Prostate Cancer Disparities and Management in Southern Africa: Insights into Practices, Norms and Values.Cancer management and research · 2022Review
- Potential Role and Clinical Value of PPP2CA in Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2021Article
- A radiosensitizer, gallotannin-rich extract from Bouea macrophylla seeds, inhibits radiation-induced epithelial-mesenchymal transition in breast cancer cells.BMC complementary medicine and therapies · 2021Article
- Prediction of tumor location in prostate cancer tissue using a machine learning system on gene expression data.BMC bioinformatics · 2020Article
- Therapies Targeted to Androgen Receptor Signaling Axis in Prostate Cancer: Progress, Challenges, and Hope.Cancers · 2019Review
- CDK7 Inhibition Suppresses Castration-Resistant Prostate Cancer through MED1 Inactivation.Cancer discovery · 2019Article
- Review
- Small-Molecule Activators of Protein Phosphatase 2A for the Treatment of Castration-Resistant Prostate Cancer.Cancer research · 2018Article
- Article
- PP2A as the Main Node of Therapeutic Strategies and Resistance Reversal in Triple-Negative Breast Cancer.Molecules (Basel, Switzerland) · 2017Review
- OP449 inhibits breast cancer growth without adverse metabolic effects.Endocrine-related cancer · 2017Article
- Genetic variants in PPP2CA are associated with gastric cancer risk in a Chinese population.Scientific reports · 2017Article
- Role of 20-Hydroxyeicosatetraenoic Acid (20-HETE) in Androgen-Mediated Cell Viability in Prostate Cancer Cells.Hormones & cancer · 2017Article
- All roads lead to PP2A: exploiting the therapeutic potential of this phosphatase.The FEBS journal · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Earlier we identified PPP2CA, which encodes for the α-isoform of protein phosphatase 2A (PP2A) catalytic subunit, as one of the downregulated genes in androgen-independent prostate cancer. PP2A is a serine/threonine phosphatase and a potent tumor suppressor involved in broad cellular functions; however, its role in prostate cancer has not yet been determined. Here, we have investigated the effect of PP2A activity modulation on the androgen-independent growth of prostate cancer cells. Our data show that the PPP2CA expression and PP2A activity is downregulated in androgen-independent (C4-2) prostate cancer cells as compared with androgen-dependent (LNCaP) cells. Downregulation of PP2A activity by pharmacologic inhibition or short interfering RNA-mediated PPP2CA silencing sustains the growth of LNCaP cells under an androgen-deprived condition by relieving the androgen deprivation-induced cell-cycle arrest and preventing apoptosis. Immunoblot analyses reveal enhanced phosphorylation of Akt, extracellular signal-regulated kinase (ERK), BAD, increased expression of cyclins (A1/D1), and decreased expression of cyclin inhibitor (p27) on PP2A downregulation. Furthermore, our data show that androgen receptor (AR) signaling is partially maintained in PP2A-inhibited cells through increased AR expression and ligand-independent phosphorylation. Pharmacologic inhibition of Akt, ERK, and AR suggest a role of these signaling pathways in facilitating the androgen-independent growth of LNCaP cells. These observations are supported by the effect of ceramide, a PP2A activator, on androgen-independent C4-2 cells. Ceramide inhibited the growth of C4-2 cells on androgen deprivation, an effect that could be abrogated by PP2A downregulation. Altogether, our findings suggest that modulation of PP2A activity may represent an alternative therapeutic approach for the treatment of advanced androgen-independent prostate cancer.
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