ArticleAmerican journal of translational research2020
Glioma-associated oncogene homolog 1 stimulates FOXP3 to promote non-small cell lung cancer stemness.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Tumor cell-specific exon 3-deleted FOXP3 isoform promotes growth and metastasis via STAT3 in non-small cell lung cancer.Life medicine · 2026Article
- Review
- Transcriptional activation of Proteasome 26S non-ATPase subunit 7 by forkhead box P3 participates in gastric cancer cell proliferation and apoptosis.Bioengineered · 2022Article
- HDAC6/FOXP3/HNF4α axis promotes bile acids induced gastric intestinal metaplasia.American journal of cancer research · 2022Article
- Forkhead Box Protein P3 (FOXP3) Represses ATF3 Transcriptional Activity.International journal of molecular sciences · 2021Article
- SOX2 Regulates lncRNA CCAT1/MicroRNA-185-3p/FOXP3 Axis to Affect the Proliferation and Self-Renewal of Cervical Cancer Stem Cells.Nanoscale research letters · 2021Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma-associated oncogene homolog 1 (GLI1), an oncogenic molecule in non-small cell lung cancer (NSCLC), promotes the growth of NSCLC by enhancing lung cancer stem cells (LCSCs). However, the mechanism responsible remains unknown. FOXP3 is known to maintain LCSCs. The aim of this study was to explore whether GLI1 enhanced LCSCs via stimulating FOXP3. Experiments were performed in NSCLC tissue samples, cell lines and the animal tumor model. The expression of GLI1- and LCSC-related molecules was assessed at protein and mRNA levels. Relevant cell functions were also determined. A tumor xenograft mouse model was established to confirm the oncogenic role of GLI1. We confirmed that the expression of GLI1 was up-regulated in the tumor tissues of NSCLC compared with adjacent non-tumor tissues. But no significant association between GLI1 and clinicopathological characteristics was found. GLI1 expression was positively correlated with FOXP3 and it could promote FOXP3 expression likely via acting on the promoter of FOXP3. Along with the upregulation of FOXP3, GLI1 increased the expression of LCSC markers, ALDH1A1 and OCT4A, and the formation of tumor spheres, whereas the inhibition of GLI1 decreased the above features. We also found the involvement of Notch1 activation in GLI1-mediated FOXP3 pathway. The
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Identifiers
32509180PMC7270000W3033699173What 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.