ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2020
Gefitinib promotes CXCR4-dependent epithelial to mesenchymal transition via TGF-β1 signaling pathway in lung cancer cells harboring EGFR mutation.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- The clinicopathological and prognostic value of CXCR4 expression in patients with lung cancer: a meta-analysis.BMC cancer · 2022Pooled it
- CXCR4: A Promising Novel Strategy for Lung Cancer Treatment.Biomolecules · 2026Review
- G protein-coupled receptors as novel therapeutic targets in non-small-cell lung cancer.Medical review (2021) · 2025Review
- Expression of CXCR4 in the Primary Lesion of Recurrent Metastatic Breast Cancer and Its Association With Prognosis.International journal of general medicine · 2025Article
- Proactive and reactive roles of TGF-β in cancer.Seminars in cancer biology · 2023Review
- Changes of tumor microenvironment in non-small cell lung cancer after TKI treatments.Frontiers in immunology · 2023Review
- CXCR4 promotes gefitinib resistance of Huh7 cells by activating the c-Met signaling pathway.FEBS open bio · 2021Article
- Tumor immune microenvironment in epidermal growth factor receptor-mutated non-small cell lung cancer before and after epidermal growth factor receptor tyrosine kinase inhibitor treatment: a narrative review.Translational lung cancer research · 2021Review
- Chemokine signaling in cancer-stroma communications.Journal of cell communication and signaling · 2021Review
- Epigenetic Silencing of LMX1A Contributes to Cancer Progression in Lung Cancer Cells.International journal of molecular sciences · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
purposeEpithelial to mesenchymal transition (EMT) plays an important role in acquired resistance to gefitinib in lung cancer. This study aimed to explore the underlying mechanism of gefitinib-induced EMT in lung adenocarcinoma cells harboring EGFR mutation.
methodsCXC chemokine receptor 4 (CXCR4) expression was determined through qRT-PCR, Western blot and flow cytometry assays in lung cancer cell line (PC9) bearing mutated EGFR. Functional role of CXCR4 was inhibited applying siRNAs as well as the specific antagonist AMD3100. The expression of EMT markers was determined, and the migration of PC9 cells was measured with transwell assay.
resultsWe found that gefitinib promoted the migratory capacity of PC9 cells in vitro, which correlated with EMT occurrence through upregulation of CXCR4. Blocking CXCR4 significantly suppressed gefitinib-induced enhancement of migration and EMT. Moreover, we determined that the upregulation of CXCR4 by gefitinib was dependent on TGF-β1/Smad2 signaling activity.
conclusionsOur study suggested a potential mechanism by which gefitinib induced EMT in cells harboring EGFR mutation through a pathway involving TGF-β1 and CXCR4. Thus, the combination of CXCR4 antagonist and TGFβR inhibitors might provide an alternative strategy to overcome progression of lung cancer after gefitinib treatment.
Indexed as
Identifiers
What OpenQuestion holds
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.