ArticleScientific reports2016
PI3 Kinase Pathway and MET Inhibition is Efficacious in Malignant Pleural Mesothelioma.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Repurposing of c-MET Inhibitor Tivantinib Inhibits Pediatric Neuroblastoma Cellular Growth.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Differential expression ofTranslational lung cancer research · 2024Article
- Review
- Defining and targeting tumor-associated macrophages in malignant mesothelioma.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Expression of phosphorylated ribosomal protein S6 in mesothelioma patients - correlation with clinico-pathological characteristics and outcome: results from the European Thoracic Oncology Platform (ETOP) Mesoscape project.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- DNA repair and damage pathways in mesothelioma development and therapy.Cancer cell international · 2022Review
- Protein Phosphatase 2A as a Therapeutic Target in Small Cell Lung Cancer.Molecular cancer therapeutics · 2021Article
- The influence of PI3K inhibition on the radiotherapy response of head and neck cancer cells.Scientific reports · 2020Article
- Review
- Sequencing and curation strategies for identifying candidate glioblastoma treatments.BMC medical genomics · 2019Article
- The Immune Microenvironment in Mesothelioma: Mechanisms of Resistance to Immunotherapy.Frontiers in oncology · 2019Review
- A subgroup of pleural mesothelioma expresses ALK protein and may be targetable by combined rapamycin and crizotinib therapy.Oncotarget · 2018Article
- Focal adhesion kinase a potential therapeutic target for pancreatic cancer and malignant pleural mesothelioma.Cancer biology & therapy · 2018Article
- Novel systemic therapy against malignant pleural mesothelioma.Translational lung cancer research · 2017Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant pleural mesothelioma (MPM) is an aggressive cancer that is commonly associated with prior asbestos exposure. Receptor tyrosine kinases (RTKs) such as MET and its downstream target PI3K are overexpressed and activated in a majority of MPMs. Here, we studied the combinatorial therapeutic efficacy of the MET/ALK inhibitor crizotinib, with either a pan-class I PI3K inhibitor, BKM120, or with a PI3K/mTOR dual inhibitor, GDC-0980, in mesothelioma. Cell viability results showed that MPM cells were highly sensitive to crizotinib, BKM120 and GDC-0980 when used individually and their combination was more effective in suppressing growth. Treatment of MPM cells with these inhibitors also significantly decreased cell migration, and the combination of them was synergistic. Treatment with BKM120 alone or in combination with crizotinib induced G2-M arrest and apoptosis. Both crizotinib and BKM120 strongly inhibited the activity of MET and PI3K as evidenced by the decreased phosphorylation of MET, AKT and ribosomal S6 kinase. Using a PDX mouse model, we showed that a combination of crizotinib with BKM120 was highly synergetic in inhibiting MPM tumor growth. In conclusion our findings suggest that dual inhibition of PI3K and MET pathway is an effective strategy in treating MPM as compared to a single agent.
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