ArticleCell cycle (Georgetown, Tex.)2015
BCR-ABL inactivates cytosolic PTEN through Casein Kinase II mediated tail phosphorylation.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Synthetic lethal approaches to target cancers with loss of PTEN function.Genes & diseases · 2023Article
- Novel effect of the high risk-HPV E7 CKII phospho-acceptor site on polarity protein expression.BMC cancer · 2022Article
- NCAPG promotes the proliferation of hepatocellular carcinoma through the CKII-dependent regulation of PTEN.Journal of translational medicine · 2022Article
- Case report: Active clinical manifestation of endocardial fibroelastosis in adolescence in a patient with mitral and aortic obstruction-histologic presence of endothelial-to-mesenchymal transformation.Frontiers in cardiovascular medicine · 2022Article
- Inference of kinase-signaling networks in human myeloid cell line models by Phosphoproteomics using kinase activity enrichment analysis (KAEA).BMC cancer · 2021Article
- Current Views on the Interplay between Tyrosine Kinases and Phosphatases in Chronic Myeloid Leukemia.Cancers · 2021Review
- KDM5B Is Essential for the Hyperactivation of PI3K/AKT Signaling in Prostate Tumorigenesis.Cancer research · 2020Article
- Tumor Suppressors in Chronic Lymphocytic Leukemia: From Lost Partners to Active Targets.Cancers · 2020Review
- Review
- Role of protein kinase CK2 in antitumor drug resistance.Journal of experimental & clinical cancer research : CR · 2019Review
- Everolimus in combination with Imatinib overcomes resistance in Chronic myeloid leukaemia.Medical oncology (Northwood, London, England) · 2019Article
- Strategies For Targeting Chronic Myeloid Leukaemia Stem Cells.Blood and lymphatic cancer : targets and therapy · 2019Review
- Therapeutic targeting of CK2 in acute and chronic leukemias.Leukemia · 2018Review
- PTEN proteoforms in biology and disease.Cellular and molecular life sciences : CMLS · 2017Review
- IκB-α: At the crossroad between oncogenic and tumor-suppressive signals.Oncology letters · 2017Article
- New insights on thyroid hormone mediated regulation of herpesvirus infections.Cell & bioscience · 2017Review
- The non-genomic loss of function of tumor suppressors: an essential role in the pathogenesis of chronic myeloid leukemia chronic phase.BMC cancer · 2016Review
- Article
- The Role of PTEN in Myeloid Malignancies.Hematology reports · 2015Review
- Non genomic loss of function of tumor suppressors in CML: BCR-ABL promotes IκBα mediated p53 nuclear exclusion.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressive function of PTEN is exerted within 2 different cellular compartments. In the cytosol-membrane, it negatively regulates PI3K-AKT pathway through the de-phosphorylation of phosphatidylinositol (3,4,5)-triphosphate (PIP3), therefore blocking one of the major signaling transduction pathways in tumorigenesis. In the nucleus, PTEN controls genomic stability and cellular proliferation through phosphatase independent mechanisms. Importantly, impairments in PTEN cellular compartmentalization, changes in protein levels and post-transductional modifications affect PTEN tumor suppressive functions. Targeting mechanisms that inactivate PTEN promotes apoptosis induction of cancer cells, without affecting normal cells, with appealing therapeutic implications. Recently, we have shown that BCR-ABL promotes PTEN nuclear exclusion by favoring HAUSP mediated PTEN de-ubiquitination in Chronic Myeloid Leukemia. Here, we show that nuclear exclusion of PTEN is associated with PTEN inactivation in the cytoplasm of CML cells. In particular, BCR-ABL promotes Casein Kinase II-mediated PTEN tail phosphorylation with consequent inhibition of the phosphatase activity toward PIP3. Targeting Casein Kinase II promotes PTEN reactivation with apoptosis induction. We therefore propose a novel BCR-ABL/CKII/PTEN pathway as a potential target to achieve synthetic lethality with tyrosine kinase inhibitors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.