ArticleAmerican journal of translational research2019
Snail expression contributes to temozolomide resistance in glioblastoma.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Drug resistance biomarkers in ovarian cancer: a bibliometric study from 2017 to 2022.Frontiers in oncology · 2024Pooled it
- Decoding the Snail transcriptional network: its role in cancer progression and therapy.Biology direct · 2026Review
- Role of STAT3 in cancer cell epithelial‑mesenchymal transition (Review).International journal of oncology · 2024Review
- Role of Non-Coding RNAs in TGF-β Signalling in Glioma.Brain sciences · 2023Review
- Identification of Prominent Genes between 3D Glioblastoma Models and Clinical Samples via GEO/TCGA/CGGA Data Analysis.Biology · 2023Article
- MicroRNA-221 promotes tumor progression by targeting HHIP in human glioblastoma.Translational cancer research · 2021Article
- SNAIL1: Linking Tumor Metastasis to Immune Evasion.Frontiers in immunology · 2021Review
- Mechanisms of temozolomide resistance in glioblastoma - a comprehensive review.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- Review
- Knockdown of DEPDC1B inhibits the development of glioblastoma.Cancer cell international · 2020Article
- Epithelial-Mesenchymal Transition: Role in Cancer Progression and the Perspectives of Antitumor Treatment.Acta naturaeArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is one of most malignancy tumors worldwide. Temozolomide (TMZ) is an important chemotherapy drug in GBM therapy. However, acquired TMZ-resistance frequently happens in GBM therapy and leads to high percentage of GBM recurrence. In our study, we demonstrated that Snail is upregulated in recurrent GBM tumors, and promotes the GBM cells resistant to TMZ induced apoptosis. Enhanced expression of Snail compromises the apoptosis induced by TMZ, and increases the cell migration and invasion. Reversely, depletion of Snail by siRNA has the opposite effects. In addition, we confirmed that the expression of Snail is modulated by STAT3 activation, since phospho-STAT3 level is relatively higher in recurrent GBM tumors and TMZ resistant cells. Knockdown of STAT3 turns down the expression of Snail in protein and mRNA level, and thereby sensitized the resistant GBM cells to TMZ treatment. Interestingly, the activation of STAT3 in GBM resistant cells is modulated by IL-6 secretion. Suppression of IL-6 abandons the STAT3 activation, and reduces its binding with Snail promoter. Inhibition of IL-6 by its antibody enhanced the killing effects of TMZ both in vivo and in vitro. Overall, our results provided a rational to overcome the TMZ resistant in GBM treatment by targeting IL-6-STAT3-Snail pathway.
Indexed as
Identifiers
31396334PMC6684932W2998544161What 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.