ArticleJournal of biomedical science2015
Sulforaphane attenuates EGFR signaling in NSCLC cells.
Article in Journal of biomedical science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 37 citations in OpenAlex.
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- The Anticancer Potential of Plant-Derived Nutraceuticals via the Modulation of Gene Expression.Plants (Basel, Switzerland) · 2022Review
- Efficacy of EGFR-TKI sequential therapy in patients withWorld journal of clinical cases · 2022Article
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- The disruption of protein-protein interactions with co-chaperones and client substrates as a strategy towards Hsp90 inhibition.Acta pharmaceutica Sinica. B · 2021Review
- Derivation of stationary distributions of biochemical reaction networks via structure transformation.Communications biology · 2021Article
- Profiling of subcellular EGFR interactome reveals hnRNP A3 modulates nuclear EGFR localization.Oncogenesis · 2020Article
- Hydroxygenkwanin Suppresses Non-Small Cell Lung Cancer Progression by Enhancing EGFR Degradation.Molecules (Basel, Switzerland) · 2020Article
- Heterogeneous Nuclear Ribonucleoproteins A1 and A2 Function in Telomerase-Dependent Maintenance of Telomeres.Cancers · 2019Article
- Sulforaphane suppresses EMT and metastasis in human lung cancer through miR-616-5p-mediated GSK3β/β-catenin signaling pathways.Acta pharmacologica Sinica · 2017Article
- Impact of Diet and Nutrition on Cancer Hallmarks.Journal of cancer prevention & current research · 2017Article
- Sulforaphane induces apoptosis and inhibits invasion in U251MG glioblastoma cells.SpringerPlus · 2016Article
- The Chemopreventive Phytochemical Moringin Isolated from Moringa oleifera Seeds Inhibits JAK/STAT Signaling.PloS one · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEGFR, a receptor tyrosine kinase (RTK), is frequently overexpressed and mutated in non-small cell lung cancer (NSCLC). Tyrosine kinase inhibitors (TKIs) have been widely used in the treatment of many cancers, including NSCLC. However, intrinsic and acquired resistance to TKI remains a common obstacle. One strategy that may help overcome EGFR-TKI resistance is to target EGFR for degradation. As EGFR is a client protein of heat-shock protein 90 (HSP90) and sulforaphane is known to functionally regulate HSP90, we hypothesized that sulforaphane could attenuate EGFR-related signaling and potentially be used to treat NSCLC.
resultsOur study revealed that sulforaphane displayed antitumor activity against NSCLC cells both in vitro and in vivo. The sensitivity of NSCLC cells to sulforaphane appeared to positively correlate with the inhibition of EGFR-related signaling, which was attributed to the increased proteasomal degradation of EGFR. Combined treatment of NSCLC cells with sulforaphane plus another HSP90 inhibitor (17-AAG) enhanced the inhibition of EGFR-related signaling both in vitro and in vivo.
conclusionsWe have shown that sulforaphane is a novel inhibitory modulator of EGFR expression and is effective in inhibiting the tumor growth of EGFR-TKI-resistant NSCLC cells. Our findings suggest that sulforaphane should be further explored for its potential clinical applications against NSCLC.
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