ArticleJournal of thoracic disease2018
miR-497 may enhance the sensitivity of non-small cell lung cancer cells to gefitinib through targeting the insulin-like growth factor-1 receptor.
Article in Journal of thoracic disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- IGF-1R inhibitors in cancer: A review of available evidence and future outlook.Critical reviews in oncology/hematology · 2025Review
- MonitoringFrontiers in oncology · 2023Review
- Article
- MicroRNAs as the critical regulators of tyrosine kinase inhibitors resistance in lung tumor cells.Cell communication and signaling : CCS · 2022Review
- miR-497 inhibits proliferation and invasion in triple-negative breast cancer cells via YAP1.Oncology letters · 2021Article
- The miR‑625‑3p/AXL axis induces non‑T790M acquired resistance to EGFR‑TKI via activation of the TGF‑β/Smad pathway and EMT in EGFR‑mutant non‑small cell lung cancer.Oncology reports · 2020Article
- miR-762 activation confers acquired resistance to gefitinib in non-small cell lung cancer.BMC cancer · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecently, studies have demonstrated that microRNA-497 (miR-497) plays an important role in modulating tumor cell sensitivity to chemotherapeutic drugs; however, its role in cellular resistance to the effects of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in treatment of non-small cell lung cancer (NSCLC) is not fully understood. In this study, we explored the potential of miR-497 in targeting the insulin-like growth factor-1 receptor (IGF-1R) signaling pathways to overcome gefitinib resistance.
methodsA gefitinib resistant human lung adenocarcinoma A549 cell line (A549/GR) was established by the method of gefitinib mutagenesis culture. Next, the A549/GR cells were transfected with miR-497 mimics to establish an miR-497 overexpression model, designated A549/GR-miR497-mimic. MTT assay was used to assess cell resistance to gefitinib, and western blot assay was employed to evaluate alterations of IGF-1R and the AKT1 signaling pathway.
resultsWe found that A549/GR-miR497-mimic cells (IC50 =33.76±0.97 µmol/L) were more sensitive to gefitinib than the control group (P<0.01). In addition, the expression levels of IGF-1R and phosphorylated AKT1 (p-AKT1) in A549/GR-miR497-mimic cells were reduced.
conclusionsWe demonstrated that miR-497 may have the effect of reversing gefitinib resistance and increasing the sensitivity of NSCLC cells to EGFR-TKIs by inhibiting the expression of IGF-1R and reducing activation of the downstream AKT signaling pathway. Thus, miR-497 plays a vital role in the acquired resistance to EGFR-TKIs, and it may represent a potential therapeutic strategy to treat NSCLC exhibiting resistance to EGFR-TKIs.
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