ArticleOncotarget2013
Epidermal growth factor receptor tyrosine kinase inhibition up-regulates interleukin-6 in cancer cells and induces subsequent development of interstitial pneumonia.
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- IL‑6: A key player in the EGFR‑TKI‑resistant tumor microenvironment and its therapeutic implications (Review).International journal of oncology · 2026Review
- Drug-induced interstitial lung disease caused by gefitinib in the treatment of non-small cell lung cancer: A case report.Molecular and clinical oncology · 2025Article
- Article
- Risk of interstitial lung disease in non-small cell lung cancer treated with EGFR-TKI: a real-world pharmacovigilance study.Frontiers in pharmacology · 2025Article
- Cyclophosphamide for anticancer therapy-induced interstitial lung disease in the modern era: a retrospective cohort study.Frontiers in oncology · 2025Article
- Almonertinib-induced interstitial lung disease in an NSCLC patient co-harboring EGFR Ex19del mutation and METFrontiers in oncology · 2025Article
- Article
- Molecular and Clinical Features of EGFR-TKI-Associated Lung Injury.International journal of molecular sciences · 2021Review
- EGFR inhibition blocks cancer stem cell clustering and lung metastasis of triple negative breast cancer.Theranostics · 2021Article
- EGFR-Dependent Extracellular Matrix Protein Interactions Might Light a Candle in Cell Behavior of Non-Small Cell Lung Cancer.Frontiers in oncology · 2021Review
- Tyrosine kinase inhibitors interstitial pneumonitis: diagnosis and management.Translational lung cancer research · 2019Article
- Interstitial pneumonia suspected during regorafenib administration and exacerbated by subsequent therapy with lenvatinib for unresectable hepatocellular carcinoma.Clinical journal of gastroenterology · 2019Article
- Constitutive activation of EGFR is associated with tumor progression and plays a prominent role in malignant phenotype of chondrosarcoma.Oncotarget · 2019Article
- Fibrinogen is associated with EGFR mutation status and lymphatic metastasis in non-small cell lung cancer.Oncology letters · 2019Article
- Suppression of c-MET overcomes erlotinib resistance in tongue cancer cells.OncoTargets and therapy · 2018Article
- JAK1/STAT3 Activation through a Proinflammatory Cytokine Pathway Leads to Resistance to Molecularly Targeted Therapy in Non-Small Cell Lung Cancer.Molecular cancer therapeutics · 2017Article
- Targeting non-canonical autophagy overcomes erlotinib resistance in tongue cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Metformin attenuates gefitinib-induced exacerbation of pulmonary fibrosis by inhibition of TGF-β signaling pathway.Oncotarget · 2015Article
- Lapatinib increases motility of triple-negative breast cancer cells by decreasing miRNA-7 and inducing Raf-1/MAPK-dependent interleukin-6.Oncotarget · 2015Article
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute interstitial pneumonia is one of serious side effects of epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) treatment, while it often has significant clinical benefit in cancer patients. Therefore, it is necessary to clarify underlying mechanisms for the development of the adverse effects by EGFR-TKI. In the present study, we attempted to determine how EGFR-TKI treatment in cancer cells induced interstitial pneumonia. The growth of tongue cancer HSC-3 and lung cancer A549 cell lines treated with EGFR-TKI was assessed by MTT assay. Cytokines and growth factors in conditioned medium (CM) obtained from EGFR-TKI-treated cancer cells were analyzed using cytokine membrane array and ELISA. Interleukin-6 (IL-6) promoter activity was measured by luciferase assay. We found that EGFR-TKI treatment significantly decreased the cell viability yet increased expression levels of IL-6 protein and mRNA, IL-6 secretion, and IL-6 transcriptional activity in these lines. In addition, using the co-culture model and IL-6 treatment was found to increase the expression of collagen and α-actin, which were markers for fibrosis, in lung fibroblast cells. These results suggest that up-regulated IL-6 plays an important role in the development of EGFR-TKI-induced interstitial fibroblastic proliferation. Therefore, blocking of IL-6 signaling could be beneficial to cancer patients undergoing EGFR-TKI treatment for reducing the risk of its unfavorable effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.