ArticleMolecular medicine reports2018
Shikonin sensitizes wild‑type EGFR NSCLC cells to erlotinib and gefitinib therapy.
Article in Molecular medicine reports, 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, 26 citations in OpenAlex.
- Exosomal circPOLK promotes metastasis of NSCLC cells via regulating mir-1204/SOX8 axis.Cancer cell international · 2026Article
- Natural compounds for non-small cell lung cancer treatment: focus on the EGFR signaling pathway.Frontiers in pharmacology · 2026Review
- BRG1 (SMARCA4) Status Dictates the Response to EGFR Inhibitors in Wild-Type EGFR Non-Small Cell Lung Cancer.Cancers · 2025Article
- Thermal cycling‑hyperthermia sensitizes non‑small cell lung cancer A549 cells to EGFR tyrosine kinase inhibitor erlotinib.Oncology reports · 2025Article
- Endoplasmic reticulum stress in non-small cell lung cancer: a review of therapeutic agents, mechanistic insights, and implications for therapy.Frontiers in cell and developmental biology · 2025Review
- Shikonin induces the apoptosis and pyroptosis of EGFR-T790M-mutant drug-resistant non-small cell lung cancer cells via the degradation of cyclooxygenase-2.European journal of medical research · 2024Article
- Impact of CD151 overexpression on prognosis and therapy in non-small cell lung cancer patients lacking EGFR mutations.Cell proliferation · 2024Article
- Promoting reactive oxygen species accumulation to overcome tyrosine kinase inhibitor resistance in cancer.Cancer cell international · 2024Review
- Shikonin Causes an Apoptotic Effect on Human Kidney Cancer Cells through Ras/MAPK and PI3K/AKT Pathways.Molecules (Basel, Switzerland) · 2023Article
- Development and validation of a prognosis prediction model based on 18 endoplasmic reticulum stress-related genes for patients with lung adenocarcinoma.Frontiers in oncology · 2022Article
- Anticancer Effects of Amlodipine Alone or in Combination With Gefitinib in Non-Small Cell Lung Cancer.Frontiers in pharmacology · 2022Article
- Medicinal herbs and bioactive compounds overcome the drug resistance to epidermal growth factor receptor inhibitors in non-small cell lung cancer.Oncology letters · 2021Review
- Resveratrol sensitizes A549 cells to irradiation damage via suppression of store-operated calcium entry with Orai1 and STIM1 downregulation.Experimental and therapeutic medicine · 2021Article
- Endoplasmic Reticulum Stress Contributes to Gefitinib-Induced Apoptosis in Glioma.International journal of molecular sciences · 2021Article
- Liraglutide attenuates gefitinib-induced cardiotoxicity and promotes cardioprotection through the regulation of MAPK/NF-κB signaling pathways.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020Article
- Experimental Study of Hepatocellular Carcinoma Treatment by Shikonin Through Regulating PKM2.Journal of hepatocellular carcinoma · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As patients with non‑small cell lung cancer (NSCLC) and wild‑type epidermal growth factor receptor (EGFR) are resistant to treatment with erlotinib or gefitinib, potential chemosensitizers are required to potentiate wild‑type EGFR NSCLC cells to erlotinib/gefitinib treatment. The present study reported that shikonin could sensitize the anticancer activity of erlotinib/gefitinib in wild‑type EGFR NSCLC cells. Furthermore, shikonin could potentiate mitochondrial‑mediated apoptosis induced by erlotinib/gefitinib in wild‑type EGFR NSCLC cells. In addition, the present study demonstrated that shikonin could induce apoptosis by activating reactive oxygen species (ROS)‑mediated endoplasmic reticulum (ER) stress, and that erlotinib/gefitinib may also induce ER stress in wild‑type EGFR NSCLC cells; however, shikonin plus erlotinib/gefitinib was more effective in activating ER stress than either agent alone. This indicated that ROS‑mediated ER stress may be associated with enhanced mitochondrial apoptosis induced by shikonin plus erlotinib/gefitinib. In addition, shikonin may promote the transition of cytoprotective ER stress‑inducing EGFR‑tyrosine kinase inhibitor tolerance to apoptosis‑promoting ER stress. Furthermore, shikonin may enhance the anti‑NSCLC activity of erlotinib/gefitinib in vivo. The data of the present study indicated that shikonin may be a potential sensitizer to enhance the anti‑cancer efficacy of erlotinib/gefitinib in wild‑type EGFR NSCLC cells resistant to erlotinib/gefitinib treatment.
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