ArticleCancer management and research2019
Novel Hsp90 Inhibitor C086 Potently Inhibits Non-Small Cell Lung Cancer Cells As A Single Agent Or In Combination With Gefitinib.
Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Heat shock proteins as hallmarks of cancer: insights from molecular mechanisms to therapeutic strategies.Journal of hematology & oncology · 2024Review
- Glucuronic acid metabolites of phenolic acids target AKT-PH domain to improve glucose metabolism.Chinese herbal medicines · 2023Article
- Enhanced anti-hepatoma effect of a novel curcumin analog C086Drug delivery · 2020Article
- DRP1 promotes lactate utilization in KRAS-mutant non-small-cell lung cancer cells.Cancer science · 2020Article
- Heat Shock Proteins and PD-1/PD-L1 as Potential Therapeutic Targets in Myeloproliferative Neoplasms.Cancers · 2020Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeInhibition of heat shock protein 90 (Hsp90) can lead to degradation of multiple client proteins, which are involved in tumor progression. Elevated Hsp90 expression has been linked to poor prognosis in patients with non-small cell lung cancer (NSCLC). Discovery of effective drug is a promising strategy to improve patient survival. This study aims to investigate the synergistic antitumor mechanism of C086 combined with gefitinib in NSCLC cells in vitro.
methodsThe binding of C086, gefitinib, and the combinations to Hsp90 was characterized by fluorescence quenching experiments. The inhibition of A549 or NCI-H1975 cell proliferation and apoptosis by C086 and gefitinib as a single agent or in combinations were performed using CFSE staining assays, AnnexinV-APC/PI and Western blot.
resultsC086 alone or with gefitinib reduces proliferation and increases proapoptotic caspase activation of both wild-type and mutation NSCLC, with NCI-H1975 cells showing much greater sensitivity to C086 and the combinations than A549 cells. The combination of C086 and gefitinib showed synergistic reduction of EGFR expression and the downstream PI3K/Akt and Ras-Raf-Erk pathways enhanced suppression of Erk signaling.
conclusionC086 combined gefitinib has a good synergistic antitumor effect in vitro. Therefore, the combination of C086 and gefitinib may provide a new theoretical basis and ideas for the treatment of NSCLC patients.
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