ArticleClinical cancer research : an official journal of the American Association for Cancer Research2014
Molecular pathways: PI3K pathway phosphatases as biomarkers for cancer prognosis and therapy.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Phospho-kinase profile of colorectal tumors guides in the selection of multi-kinase inhibitors.Oncotarget · 2015Trial
- Synergistic and toxicity‑reducing effects of acteoside as an adjuvant therapy of oxaliplatin against hepatocellular carcinoma.International journal of oncology · 2025Article
- Progression of the PI3K/Akt signaling pathway in chronic obstructive pulmonary disease.Frontiers in pharmacology · 2023Review
- Transcription factor SNAI2 exerts pro-tumorigenic effects on glioma stem cells via PHLPP2-mediated Akt pathway.Cell death & disease · 2022Article
- Predicting the Lung Adenocarcinoma and Its Biomarkers by Integrating Gene Expression and DNA Methylation Data.Frontiers in genetics · 2022Article
- CircIL4R activates the PI3K/AKT signaling pathway via the miR-761/TRIM29/PHLPP1 axis and promotes proliferation and metastasis in colorectal cancer.Molecular cancer · 2021Article
- Prognostic value of theArchives of medical science : AMS · 2021Article
- LncRNA GAS5/miR-137 Is a Hypoxia-Responsive Axis Involved in Cardiac Arrest and Cardiopulmonary Cerebral Resuscitation.Frontiers in immunology · 2021Article
- Dexamethasone Interferes with Autophagy and Affects Cell Survival in Irradiated Malignant Glioma Cells.Journal of Korean Neurosurgical Society · 2020Article
- Investigating the duality ofOncotarget · 2019Article
- Inositol polyphosphate 4-phosphatase type II regulation of androgen receptor activity.Oncogene · 2019Article
- Drug Resistance in HER2-Positive Breast Cancer Brain Metastases: Blame the Barrier or the Brain?Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
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- Overexpression of CAPN2 promotes cell metastasis and proliferation via AKT/mTOR signaling in renal cell carcinoma.Oncotarget · 2017Article
- Molecular mechanisms underlying Th1-like Treg generation and function.Cellular and molecular life sciences : CMLS · 2017Review
- Musashi-1 promotes a cancer stem cell lineage and chemoresistance in colorectal cancer cells.Scientific reports · 2017Article
- Silencing CAPN2 Expression Inhibited Castration-Resistant Prostate Cancer Cells Proliferation and Invasion via AKT/mTOR Signal Pathway.BioMed research international · 2017Article
- Inactivating Frameshift Mutation of INPP4B Encoding a PI3K Pathway Phosphatase in Gastric and Colorectal Cancers.Pathology oncology research : POR · 2016Article
- MYC Drives Pten/Trp53-Deficient Proliferation and Metastasis due to IL6 Secretion and AKT Suppression via PHLPP2.Cancer discovery · 2015Article
- PTEN functions by recruitment to cytoplasmic vesicles.Molecular cell · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cancer research has seen tremendous changes over the past decade. Fast progress in sequencing technology has afforded us with landmark genetic alterations, which had immediate impact on clinical science and practice by pointing to new kinase targets, such as phosphoinositide 3-kinase (PI3K), the EGF receptor, or BRAF. The PI3K pathway for growth control has emerged as a prime example for both oncogene activation and tumor suppressor loss in cancer. Here, we discuss how therapy using PI3K pathway inhibitors could benefit from information on specific phosphatases, which naturally antagonize the kinase targets. This PI3K pathway is found mutated in most cancer types, including prostate, breast, colon, and brain tumors. The tumor-suppressing phosphatases operate at two levels. Lipid-level phosphatases, such as PTEN and INPP4B, revert PI3K activity to keep the lipid second messengers inactive. At the protein level, PHLPP1/2 protein phosphatases inactivate AKT kinase, thus antagonizing mTOR complex 2 activity. However, in contrast with their kinase counterparts the phosphatases are unlikely drug targets. They would need to be stimulated by therapy and are commonly deleted and mutated in cancer. Yet, because they occupy critical nodes in preventing cancer initiation and progression, the information on their status has tremendous potential in outcome prediction, and in matching the available kinase inhibitor repertoire with the right patients. Clin Cancer Res; 20(12); 3057-63. ©2014 AACR.
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