ArticleBritish journal of haematology2013
The phosphatidylinositol 3-kinases (PI3K) inhibitor GS-1101 synergistically potentiates histone deacetylase inhibitor-induced proliferation inhibition and apoptosis through the inactivation of PI3K and extracellular signal-regulated kinase pathways.
Article in British journal of haematology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Roles of PI3Kγ and PI3Kδ in mantle cell lymphoma proliferation and migration contributing to efficacy of the PI3Kγ/δ inhibitor duvelisib.Scientific reports · 2023Article
- A Review of Phosphocreatine 3 Kinase δ Subtype (PI3Kδ) and Its Inhibitors in Malignancy.Medical science monitor : international medical journal of experimental and clinical research · 2021Review
- Design, Synthesis, and Biological Evaluation of Quinazolin-4-one-Based Hydroxamic Acids as Dual PI3K/HDAC Inhibitors.Journal of medicinal chemistry · 2020Article
- Resistance to BTK inhibition by ibrutinib can be overcome by preventing FOXO3a nuclear export and PI3K/AKT activation in B-cell lymphoid malignancies.Cell death & disease · 2019Article
- Dual inhibition of histone deacetylases and phosphoinositide 3-kinase enhances therapeutic activity against B cell lymphoma.Oncotarget · 2017Article
- Idelalisib Impacts Cell Growth through Inhibiting Translation-Regulatory Mechanisms in Mantle Cell Lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Tris (dibenzylideneacetone) dipalladium: a small-molecule palladium complex is effective in inducing apoptosis in chronic lymphocytic leukemia B-cells.Leukemia & lymphoma · 2016Article
- [The advances of clinical and molecular prognostic factors of diffuse large B-cell lymphoma].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2016Article
- The role of idelalisib in the treatment of relapsed and refractory chronic lymphocytic leukemia.Therapeutic advances in hematology · 2016Review
- Panobinostat as Pan-deacetylase Inhibitor for the Treatment of Pancreatic Cancer: Recent Progress and Future Prospects.Oncology and therapy · 2016Review
- Therapeutic targeting of replicative immortality.Seminars in cancer biology · 2015Review
- [Advances of aberrant signaling pathways and related targeting drugs in B cell non- Hodgkin lymphoma].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2015Article
- Targeting neoplastic B cells and harnessing microenvironment: the "double face" of ibrutinib and idelalisib.Journal of hematology & oncology · 2015Review
- MCL-1 and BCL-xL-dependent resistance to the BCL-2 inhibitor ABT-199 can be overcome by preventing PI3K/AKT/mTOR activation in lymphoid malignancies.Cell death & disease · 2015Article
- The protective role of interleukin-11 against neutron radiation injury in mouse intestines via MEK/ERK and PI3K/Akt dependent pathways.Digestive diseases and sciences · 2014Article
- Idelalisib for the treatment of chronic lymphocytic leukemia.ISRN oncology · 2014Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Previously, we showed that inhibition of the protein kinase C β (PKCβ)/AKT pathway augments engagement of the histone deacetylase inhibitor (HDI)-induced apoptosis in lymphoma cells. In the present study, we investigated the cytotoxicity and mechanisms of cell death induced by the delta isoform-specific phosphatidylinositide 3-kinase (PI3K) inhibitor, GS-1101, in combination with the HDI, panobinostat (LBH589) and suberoylanilide hydroxamic acid (SAHA). Lymphoma cell lines, primary non-Hodgkin Lymphoma (NHL) and chronic lymphocytic leukaemia (CLL) cells were simultaneously treated with the HDI, LBH589 and GS-1101. An interaction of the LBH589/GS-1101 combination was formally examined by using various concentrations of LBH589 and GS-1101. Combined treatment resulted in a synergistic inhibition of proliferation and showed synergistic effect on apoptotic induction in all tested cell lines and primary NHL and CLL cells. This study indicates that interference with PI3K signalling dramatically increases HDI-mediated apoptosis in malignant haematopoietic cells, possibly through both AKT-dependent or AKT- independent mechanisms. Moreover, the increase in HDI-related apoptosis observed in PI3K inhibitor-treated cells appears to be related to the disruption of the extracellular signal-regulated kinase (ERK) signalling pathway. This study provides a strong rational for testing the combination of PI3K inhibitors and HDI in the clinic.
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