ArticleMolecular medicine reports2015
Transcription factor glioma-associated oncogene homolog 1 is required for transforming growth factor-β1-induced epithelial-mesenchymal transition of non-small cell lung cancer cells.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Gli1 promotes epithelial-mesenchymal transition and metastasis of non-small cell lung carcinoma by regulating snail transcriptional activity and stability.Acta pharmaceutica Sinica. B · 2022Article
- Glioma-associated oncogene homolog 1 stimulates FOXP3 to promote non-small cell lung cancer stemness.American journal of translational research · 2020Article
- Ursolic Acid Attenuates TGF-β1-Induced Epithelial-Mesenchymal Transition in NSCLC by Targeting Integrin αVβ5/MMPs Signaling.Oncology research · 2019Article
- Comprehensive analysis of genes based on chr1p/19q co-deletion reveals a robust 4-gene prognostic signature for lower grade glioma.Cancer management and research · 2019Article
- EMT cells increase breast cancer metastasis via paracrine GLI activation in neighbouring tumour cells.Nature communications · 2017Article
- Developmental pathways associated with cancer metastasis: Notch, Wnt, and Hedgehog.Cancer biology & medicine · 2017Article
- GANT61, a GLI inhibitor, sensitizes glioma cells to the temozolomide treatment.Journal of experimental & clinical cancer research : CR · 2016Article
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5 authors at 2 institutions in 1 country.
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Abstract
Epithelial‑mesenchymal transition (EMT) is the process by which epithelial cells depolarize and acquire a mesenchymal phenotype, and is a common early step in the process of metastasis. Patients with lung cancer frequently already have distant metastases when they are diagnosed, highlighting the requirement for early and effective interventions to control metastatic disease. Transforming growth factor‑β1 (TGF‑β1) is able to induce EMT, however the molecular mechanism of this remains unclear. In the current study, TGF‑β1 was reported to induce EMT and promote the migration of non‑small cell lung cancer (NSCLC) cells. A notable observation was that EMT induction was accompanied by the upregulation of human glioma‑associated oncogene homolog 1 (Gli1) mRNA and protein levels. Furthermore, Gli1 levels were depleted by small interfering RNA, and the Gli1 inhibitor GANT 61 attenuated the TGF‑β1‑mediated induction of EMT and cell migration. The results of the current study suggest that Gli1 regulates TGF‑β1‑induced EMT, which may provide a novel therapeutic target to inhibit metastasis in patients with NSCLC.
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