ArticlePloS one2018
NF-κB activation is an early event of changes in gene regulation for acquiring drug resistance in human adenocarcinoma PC-9 cells.
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 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Harnessing transcriptomics for discovery of natural products to overcome acquired cancer resistance.Archives of pharmacal research · 2026Review
- Characteristics and molecular mechanism of drug-tolerant cells in cancer: a review.Frontiers in oncology · 2023Review
- Cosuppression of NF-κB and AICDA Overcomes Acquired EGFR-TKI Resistance in Non-Small Cell Lung Cancer.Cancers · 2022Article
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- Review
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- miR-146b-5p Enhances the Sensitivity of NSCLC to EGFR Tyrosine Kinase Inhibitors by Regulating the IRAK1/NF-κB Pathway.Molecular therapy. Nucleic acids · 2020Article
- Small Molecule NF-κB Pathway Inhibitors in Clinic.International journal of molecular sciences · 2020Review
- Inhibition of FGF2-Mediated Signaling in GIST-Promising Approach for Overcoming Resistance to Imatinib.Cancers · 2020Review
- Transcriptome Profiling of Acquired Gefitinib Resistant Lung Cancer Cells Reveals Dramatically Changed Transcription Programs and New Treatment Targets.Frontiers in oncology · 2020Article
- Targeting the reversible drug-tolerant state: aurora kinase A, is that the final answer?Translational cancer research · 2019Article
- Aspirin suppresses chemoresistance and enhances antitumor activity of 5-Fu in 5-Fu-resistant colorectal cancer by abolishing 5-Fu-induced NF-κB activation.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gefitinib and erlotinib are epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs). Although EGFR-TKIs are effective as anti-cancer drugs, cancer cells sometimes gain tolerance to the drugs. Previous studies suggested that the fibroblast growth factor receptor (FGFR)-signaling pathway could serve as compensation for the EGFR-signaling pathway inhibited by EGFR-TKIs. Our study further suggested that FGF2, a FGFR ligand, leaked out from naïve cells killed by gefitinib could initiate the FGFR-signaling pathway in surviving cells; i.e., altruistic survival may occur in naïve cells immediately after EGFR-TKI treatment. Altruistic survival may be temporal, and cells need to change their gene regulation toward gaining resistance to EGFR-TKIs. Changes in such gene regulation after EGFR-TKI treatment are poorly understood. In this study, we examined early events of such gene regulation changes in human adenocarcinoma PC-9 cells that are capable of changing their nature from susceptibility to resistance to EFGR-TKIs. Our study indicated that activation of nuclear factor-kappa B (NF-κB) occurred in the cells immediately after EGFR-TKI treatment and also by gene silencing against oncogenic EGFR; and, MG132 treatment for inhibiting NF-κB activation affected cell viability. Taken together, our findings (including the previous study) suggest that altruistic survival and NF-κB activation might be vital for initiating the acquisition of EGFR-TKI resistance.
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