ArticleActa haematologica2014
Class IA PI3K inhibition inhibits cell growth and proliferation in mantle cell lymphoma.
Article in Acta haematologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Pan-phosphatidylinositol 3-kinase inhibition with buparlisib in patients with relapsed or refractory non-Hodgkin lymphoma.Haematologica · 2017Trial
- Huanglian Jiedu Decoction Alleviates Myocardial Ischemia-Reperfusion Injury via AKT-Mediated Regulation of Endoplasmic Reticulum Stress.Journal of inflammation research · 2025Article
- Leveraging altered lipid metabolism in treating B cell malignancies.Progress in lipid research · 2024Review
- Protein Kinase CK1α Sustains B-Cell Receptor Signaling in Mantle Cell Lymphoma.Frontiers in oncology · 2021Article
- Management of Drug Resistance in Mantle Cell Lymphoma.Cancers · 2020Review
- Copanlisib synergizes with conventional and targeted agents including venetoclax in B- and T-cell lymphoma models.Blood advances · 2020Article
- Sulodexide attenuates endoplasmic reticulum stress induced by myocardial ischaemia/reperfusion by activating the PI3K/Akt pathway.Journal of cellular and molecular medicine · 2019Article
- Protective effects ofJournal of thoracic disease · 2018Article
- Proteomic changes of CD4Experimental and therapeutic medicine · 2017Article
- LncRNA260-specific siRNA targetingJournal of thoracic disease · 2017Article
- Targeting mantle cell lymphoma metabolism and survival through simultaneous blockade of mTOR and nuclear transporter exportin-1.Oncotarget · 2017Article
- PIK3CA expression in diffuse large B cell lymphoma tissue and the effect of its knockdown in vitro.OncoTargets and therapy · 2017Article
- Dual inhibition of CDK4/Rb and PI3K/AKT/mTOR pathways by ON123300 induces synthetic lethality in mantle cell lymphomas.Leukemia · 2016Article
- Synergistic suppression of the PI3K inhibitor CAL-101 with bortezomib on mantle cell lymphoma growth.Cancer biology & medicine · 2015Article
- The novel combination of dual mTOR inhibitor AZD2014 and pan-PIM inhibitor AZD1208 inhibits growth in acute myeloid leukemia via HSF pathway suppression.Oncotarget · 2015Article
- Ribosomal Biogenesis and Translational Flux Inhibition by the Selective Inhibitor of Nuclear Export (SINE) XPO1 Antagonist KPT-185.PloS one · 2015Article
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
BACKGROUND/
aimsConstitutive activation of the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin signaling pathway preferentially occurs in aggressive blastoid variants of mantle cell lymphoma (MCL) and is implicated in the pathogenesis of this disease. In this study, we investigated the role of PI3K isoforms on proliferation of aggressive MCL cells.
methodsThe changes in cell viability, cell cycle distribution and apoptosis induction by the PI3K isoform-selective inhibitors were evaluated. The molecular basis underlying the effects of the specific inhibition of PI3K isoforms was investigated by Western blot analysis.
resultsOur results demonstrated that a class IA PI3K isoform is most commonly involved in the constitutive activation of Akt in aggressive MCL. Treatment with a p110α isoform-specific inhibitor induced prominent cell cycle arrest followed by apoptosis through complete abolishment of phosphorylated (p)-Akt and its downstream targets. An inhibitor of isoform p110δ induced moderate cell cycle arrest with downregulation of p-Akt and p-S6K. A dual inhibitor of p110α and p110δ GDC-0941 caused more prominent cell growth inhibition compared to selective p110α or p110δ inhibitors. Inhibition of the class IB PI3K isoform p110γ did not cause cell cycle arrest or induce apoptosis in MCL cells.
conclusionThese findings suggest that the therapeutic ablation of class IA PI3K may be a promising strategy for the treatment of refractory, aggressive MCL.
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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.