Targeting the PI3K/AKT Pathway for the Treatment of Prostate Cancer
Open accessAbstract
Despite recent advances in our understanding of the biological basis of prostate cancer, the management of the disease, especially in the castration-resistant phase, remains a significant challenge. Deregulation of the phosphatidylinositol 3-kinase pathway is increasingly implicated in prostate carcinogenesis. In this review, we detail the role of this pathway in the pathogenesis of prostate cancer and the rapidly evolving therapeutic implications of targeting it. In particular, we highlight the importance of the appropriate selection of agents and combinations, and the critical role of predictive and pharmocodynamic biomarkers.
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The PI3K/AKT signaling axis is critical in the tumorigenic process of prostate cancer, influencing apoptosis, proliferation, metastasis and invasion.
“The PI3K/AKT signaling axis is critical in the tumorigenic process of PCa, influencing apoptosis, proliferation, metastasis, and invasion.”
From Celastrol attenuates the invasion and migration and augments the anticancer effects of olaparib in prostate cancer (2024) · cites this paper as [35]
Activated Akt has a number of downstream effects, including survival/apoptosis evasion, proliferation, and protein synthesis/cell growth.
“Activated Akt has a number of downstream effects, including survival/apoptosis evasion, proliferation, and protein synthesis/cell growth (47).”
From Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer (2011) · cites this paper as [47]
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“The PI3K/AKT pathway, a crucial regulator of cell growth and survival, plays a significant role in both the development and therapy of PCa [34, 35].”
Background
- Authors
- Sarker, D., Reid, A. H. M., Yap, T. A., & de Bono, J. S.
- Affiliations
- Royal Marsden NHS Foundation Trust (GB)
- Authors' Affiliation: Section of Medicine and Cancer Research UK Centre for Cancer Therapeutics, The Institute of Cancer Research and Royal Marsden NHS Foundation Trust, Sutton, Surrey SM2 5PT, United Kingdom
- Venue
- Clinical Cancer Research
- Published
- 2009-07-29
- Volume
- 15
- Issue
- 15
- Pages
- 4799-4805
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- OpenAlex
- W2100237319
- Cited by
- 366
- References
- 7
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 11 · 2023: 14 · 2022: 16 · 2021: 26 · 2020: 19 · 2019: 16 · 2018: 24 · 2017: 26 · 2016: 14 · 2015: 27 · 2014: 26 · 2013: 36 · 2012: 30
- FWCI
- 4.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- NIHR Biomedical Research Centre, Royal Marsden NHS Foundation Trust/Institute of Cancer Research
- Cancer Research UK
- National Institute for Health and Care Research
- Imperial Experimental Cancer Medicine Centre
- Medical Research Council
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- PI3K/Akt signaling, prostate cancer, castration-resistant prostate cancer, phosphatidylinositol 3-kinase, targeted therapy, combination therapy, predictive biomarkers, pharmacodynamic biomarkers, prostate carcinogenesis
- MeSH terms
- Transcriptional Regulator ERG, Phosphoinositide-3 Kinase Inhibitors, Humans, Male, Prostatic Neoplasms, Receptors, Androgen, Serine Endopeptidases, Signal Transduction, Oncogene Proteins, Fusion, Trans-Activators, Chemokines, Phosphatidylinositol 3-Kinases, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, PTEN Phosphohydrolase, Androgen Receptor Antagonists
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