ArticlePloS one2018
A-674563, a putative AKT1 inhibitor that also suppresses CDK2 activity, inhibits human NSCLC cell growth more effectively than the pan-AKT inhibitor, MK-2206.
Article in PloS one, 2018. 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, 29 citations in OpenAlex.
- Cytoskeletal Protein 4.1R Inhibits BCR-Mediated B-Cell Activation by Restraining AKT1 Phosphorylation.Cells · 2026Article
- AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024Review
- Chemoresistance Mechanisms in Non-Small Cell Lung Cancer-Opportunities for Drug Repurposing.Applied biochemistry and biotechnology · 2024Review
- Involvement of the AKT Pathway in Resistance to Erlotinib and Cabozantinib in Triple-Negative Breast Cancer Cell Lines.Biomedicines · 2023Article
- Using ChEMBL to Complement Schistosome Drug Discovery.Pharmaceutics · 2023Article
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
- Article
- Cyclin B/CDK1 and Cyclin A/CDK2 phosphorylate DENR to promote mitotic protein translation and faithful cell division.Nature communications · 2022Article
- Article
- Advances in Immunosuppressive Agents Based on Signal Pathway.Frontiers in pharmacology · 2022Review
- Emerging Roles for AKT Isoform Preference in Cancer Progression Pathways.Molecular cancer research : MCR · 2021Review
- Role of AMPK and Akt in triple negative breast cancer lung colonization.Neoplasia (New York, N.Y.) · 2021Article
- Nidogen 1 regulates proliferation and migration/invasion in murine claudin-low mammary tumor cells.Oncology letters · 2021Article
- Three NovelOncoTargets and therapy · 2020Article
- Screening of the copy number increase ofInternational journal of clinical and experimental pathology · 2019Article
- The calcium channel proteins ORAI3 and STIM1 mediate TGF-β inducedOncotarget · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AKT is a serine-threonine kinase implicated in tumorigenesis as a central regulator of cellular growth, proliferation, survival, and metabolism. Activated AKT is commonly overexpressed in non-small cell lung cancer (NSCLC) and accordingly AKT inhibitors are under clinical investigation for NSCLC treatment. Thus far, the AKT inhibitors being evaluated broadly target all three (1-3) AKT isoforms but recent evidence suggests opposing roles in lung tumorigenesis where loss of Akt1 inhibits while the loss of Akt2 enhances lung tumor development. Based on these findings, we hypothesized that selective inhibition of AKT-1 would be a more effective therapeutic strategy than pan-AKT inhibition for NSCLC treatment. Using six NSCLC cell lines, we found that the AKT-1 inhibitor, A-674563, was significantly more effective at reducing NSCLC cell survival relative to the pan-AKT inhibitor MK-2206. Comparison of the downstream effects of the inhibitors suggests that altered cell cycle progression and off-target CDK2 inhibition are likely vital to the improved efficacy of A-674563 over MK-2206.
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