ArticleCell death & disease2019
Targeting the COX2/MET/TOPK signaling axis induces apoptosis in gefitinib-resistant NSCLC cells.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The trial behind it
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Advances in T-Lymphokine-activated Killer Cell-originated Protein Kinase Research in Cancer Over the Past Thirty Years.Journal of cancer prevention · 2026Review
- The Roles of TOPK in Tumorigenesis and Development: Structure, Mechanisms, Pathways, and Therapeutic Implications.International journal of biological sciences · 2026Review
- The SRC-TOPK positive feedback loop promotes RB1 phosphorylation and drives the development of lung squamous cell carcinoma.Acta biochimica et biophysica Sinica · 2025Article
- Celecoxib in oncology: targeting the COX-2/PGEFrontiers in pharmacology · 2025Review
- Combined inhibition of MET and VEGF enhances therapeutic efficacy of EGFR TKIs in EGFR-mutant non-small cell lung cancer with concomitant aberrant MET activation.Experimental hematology & oncology · 2024Article
- TOPK Inhibition Enhances the Sensitivity of Colorectal Cancer Cells to Radiotherapy by Reducing the DNA Damage Response.Current medical science · 2024Article
- Stress granules affect the sensitivity of renal cancer cells to sorafenib by sequestering and stabilizing COX‑2 mRNA.Oncology letters · 2023Article
- Review
- FYN/TOPK/HSPB1 axis facilitates the proliferation and metastasis of gastric cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- Inhibiting ALK-TOPK signaling pathway promotes cell apoptosis of ALK-positive NSCLC.Cell death & disease · 2022Article
- TOPK/PBK is phosphorylated by ERK2 at serine 32, promotes tumorigenesis and is involved in sorafenib resistance in RCC.Cell death & disease · 2022Article
- The role of T-LAK cell-originated protein kinase in targeted cancer therapy.Molecular and cellular biochemistry · 2022Review
- Licochalcone A Promotes the Ubiquitination of c-Met to Abrogate Gefitinib Resistance.BioMed research international · 2022Article
- TIP30 overcomes gefitinib resistance by regulating cytoplasmic and nuclear EGFR signaling in non-small-cell lung cancer.Cancer science · 2021Article
- Review
- Tumor necrosis factor in lung cancer: Complex roles in biology and resistance to treatment.Neoplasia (New York, N.Y.) · 2021Review
- 3-Deoxysappanchalcone Inhibits Skin Cancer Proliferation by Regulating T-Lymphokine-Activated Killer Cell-Originated Protein KinaseFrontiers in cell and developmental biology · 2021Article
- Flurbiprofen suppresses the inflammation, proliferation, invasion and migration of colorectal cancer cells via COX2.Oncology letters · 2020Article
- The molecular mechanisms of celecoxib in tumor development.Medicine · 2020Article
- Article
Corrections and comments
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Authors and funding
25 authors at 10 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MET overactivation is one of the crucial reasons for tyrosine kinase inhibitor (TKI) resistance, but the mechanisms are not wholly clear. Here, COX2, TOPK, and MET expression were examined in EGFR-activating mutated NSCLC by immunohistochemical (IHC) analysis. The relationship between COX2, TOPK, and MET was explored in vitro and ex vivo. In addition, the inhibition of HCC827GR cell growth by combining COX2 inhibitor (celecoxib), TOPK inhibitor (pantoprazole), and gefitinib was verified ex vivo and in vivo. We found that COX2 and TOPK were highly expressed in EGFR-activating mutated NSCLC and the progression-free survival (PFS) of triple-positive (COX2, MET, and TOPK) patients was shorter than that of triple-negative patients. Then, we observed that the COX2-TXA
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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.