ArticleJournal of experimental & clinical cancer research : CR2019
Cathepsin L activated by mutant p53 and Egr-1 promotes ionizing radiation-induced EMT in human NSCLC.
Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 59 citations in OpenAlex.
- Mutant p53 Regulates Pyruvate Dehydrogenase Kinase 1 (PDK1) to Promote Proliferation and Migration in Breast Cancer.Cancer science · 2026Article
- The lysosomal cysteine protease cathepsin L promotes stemness and multidrug resistance of non-small cell lung cancer by targeting HGF activator.Molecular and cellular biochemistry · 2026Article
- UCHL1 stabilizes Twist1 via K11/K63-linked deubiquitination to drive tumor metastasis in non-small cell lung cancer.Cell death discovery · 2025Article
- USP20 competitively binds to STUB1 to enhance CTSL expression and promote epithelial-mesenchymal transition in head and neck squamous cell carcinoma.Clinical and translational medicine · 2025Article
- Unveiling PANoptosis in Acute Kidney Injury: An Integrative Multi-Dimensional Approach to Identify Key Biomarkers.Journal of inflammation research · 2025Article
- USP9X inhibits metastasis in pulmonary sarcomatoid carcinoma by regulating epithelial-mesenchymal transition, angiogenesis and immune infiltration.Translational oncology · 2024Article
- Two-polarized roles of transcription factor FOSB in lung cancer progression and prognosis: dependent on p53 status.Journal of experimental & clinical cancer research : CR · 2024Article
- Egr1 regulates regenerative senescence and cardiac repair.Nature cardiovascular research · 2024Article
- Circ-10720 as a ceRNA adsorbs microRNA-1238 and modulates ZEB2 to boost NSCLC development by activating EMT.European journal of medical research · 2024Article
- Article
- Role of early growth response 1 in inflammation-associated lung diseases.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- EGR1 induces EMT in pancreatic cancer via a P300/SNAI2 pathway.Journal of translational medicine · 2023Article
- Effects of Fractionated Radiation Exposure on Vimentin Expression in Cervical Cancers: Analysis of Association with Cancer Stem Cell Response and Short-Term Prognosis.International journal of molecular sciences · 2023Article
- Article
- The Molecular and Cellular Strategies of Glioblastoma and Non-Small-Cell Lung Cancer Cells Conferring Radioresistance.International journal of molecular sciences · 2022Review
- Assessment of immune status of laryngeal squamous cell carcinoma can predict prognosis and guide treatment.Cancer immunology, immunotherapy : CII · 2022Article
- Cathepsin L promotes chemresistance to neuroblastoma by modulating serglycin.Frontiers in pharmacology · 2022Article
- Upregulation of ERK-EGR1-heparanase axis by HDAC inhibitors provides targets for rational therapeutic intervention in synovial sarcoma.Journal of experimental & clinical cancer research : CR · 2021Article
- Contribution of p53 in sensitivity to EGFR tyrosine kinase inhibitors in non-small cell lung cancer.Scientific reports · 2021Article
- Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIonizing radiation (IR) is one of the major clinical therapies of cancer, although it increases the epithelial-mesenchymal transition (EMT) of non-small cell lung cancer (NSCLC), unexpectedly. The cellular and molecular mechanisms underlying this role are not completely understood.
methodsWe used NSCLC cell lines as well as tumor specimens from 78 patients with NSCLC to evaluate p53, Cathepsin L (CTSL) and EMT phenotypic changes. Xenograft models was also utilized to examine the roles of mutant p53 (mut-p53) and CTSL in regulating IR-induced EMT of NSCLC.
resultsExpression of CTSL was markedly increased in human NSCLC tissues with mutant p53 (mut-p53), and p53 mutation positively correlated with metastasis of NSCLC patients. In human non-small cell lung cancer cell line, H1299 cells transfected with various p53 lentivirus vectors, mut-p53 could promote the invasion and motility of cells under IR, mainly through the EMT. This EMT process was induced by elevating intranuclear CTSL which was regulated by mut-p53 depending on Early growth response protein-1 (Egr-1) activation. In the subcutaneous tumor xenograft model, IR promoted the EMT of the cancer cells in the presence of mut-p53, owing to increase expression and nuclear transition of its downstream protein CTSL.
conclusionTaken together, these data reveal the role of the mut-p53/Egr-1/CTSL axis in regulating the signaling pathway responsible for IR-induced EMT.
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