ArticleOncogene2003
Preferential killing of PTEN-null myelomas by PI3K inhibitors through Akt pathway.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 52 citations in OpenAlex.
- Pathogenic signaling in multiple myeloma.Seminars in oncology · 2022Article
- Another Weapon against Cancer and Metastasis: Physical-Activity-Dependent Effects on Adiposity and Adipokines.International journal of molecular sciences · 2021Review
- Resveratrol as a new inhibitor of immunoproteasome prevents PTEN degradation and attenuates cardiac hypertrophy after pressure overload.Redox biology · 2019Article
- Selinexor synergizes with dexamethasone to repress mTORC1 signaling and induce multiple myeloma cell death.Oncotarget · 2018Article
- Bone Marrow Adipocyte: An Intimate Partner With Tumor Cells in Bone Metastasis.Frontiers in endocrinology · 2018Review
- [Research on multiple myeloma cell apoptosis by inhibition of mTORC2 and chaperon pathways].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2015Article
- A novel PI3K inhibitor PIK-C98 displays potent preclinical activity against multiple myeloma.Oncotarget · 2015Article
- The PI3K inhibitor GDC-0941 combines with existing clinical regimens for superior activity in multiple myeloma.Oncogene · 2014Article
- Identification of a promising PI3K inhibitor for the treatment of multiple myeloma through the structural optimization.Journal of hematology & oncology · 2014Article
- Circumvention of Mcl-1-dependent drug resistance by simultaneous Chk1 and MEK1/2 inhibition in human multiple myeloma cells.PloS one · 2014Article
- Article
- Widespread deregulation of phosphorylation-based signaling pathways in multiple myeloma cells: opportunities for therapeutic intervention.Molecular medicine (Cambridge, Mass.) · 2011Article
- Thalidomide decreases gelatinase production by malignant B lymphoid cell lines through disruption of multiple integrin-mediated signaling pathways.Haematologica · 2010Article
- A novel interaction between fibroblast growth factor receptor 3 and the p85 subunit of phosphoinositide 3-kinase: activation-dependent regulation of ERK by p85 in multiple myeloma cells.Human molecular genetics · 2009Article
- Loss of PTEN function may account for reduced proliferation pathway sensitivity to LY294002 in human prostate and bladder cancer cells.Journal of cancer research and clinical oncology · 2009Article
- PTEN-deficient cancers depend on PIK3CB.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- The phosphoinositide 3-kinase pathway in human cancer: genetic alterations and therapeutic implications.Current genomics · 2007Article
- Atiprimod blocks STAT3 phosphorylation and induces apoptosis in multiple myeloma cells.British journal of cancer · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently reported that internal deletion of PTEN tumor suppressor gene in OPM2 and Delta47 myeloma lines led to high Akt activation. Re-expression of PTEN induced strong apoptosis and growth inhibition. To understand the biologic importance of the phosphatidylinositol 3 kinase (PI3K)/Akt activation affected by PTEN deletion, we analysed apoptosis and growth inhibition by applying PI3K inhibitors to myeloma lines and by expressing Akt constructs. The PI3K inhibitors preferentially suppressed PTEN-null myeloma growth to those expressing PTEN, indicating that PI3K activation is more critical for growth and survival of those lines with PTEN mutations than others expressing a functional PTEN gene. Since PTEN-null myeloma lines exhibited much stronger Akt activation than PTEN-expressing cells in response to insulin-like growth factor I stimulation, we determined whether Akt could be responsible for PI3K-mediated cell survival and growth of PTEN-null myeloma lines. Expression of an active Akt, but not its kinase dead mutant, reversed wortmannin- and dexamethasone-induced apoptosis and growth inhibition in PTEN-null myeloma lines, suggesting that Akt lies downstream of PI3K for PTEN-null myeloma survival and dexamethasone resistance. In summary, we have provided evidence that PTEN-null myeloma cells are stringently dependent on the PI3K/Akt activation for cell survival. These results may provide a basis to treat myeloma patients with PI3K and Akt inhibitors.
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Registered trials
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.