ArticleCancer biomarkers : section A of Disease markers2018
Targeting signal-transducer-and-activator-of-transcription 3 sensitizes human cutaneous melanoma cells to BRAF inhibitor.
Article in Cancer biomarkers : section A of Disease markers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed.
- Exosomal CTCF Confers Cisplatin Resistance in Osteosarcoma by Promoting AutophagyJournal of oncology · 2022Article
- Non-coding RNAs in skin cancers:Biological roles and molecular mechanisms.Frontiers in pharmacology · 2022Review
- Abiraterone induces SLCO1B3 expression in prostate cancer via microRNA-579-3p.Scientific reports · 2021Article
- Review
- Expression profile and bioinformatics analysis of COMMD10 in BALB/C mice and human.Cancer gene therapy · 2020Article
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Melanoma treatment with the BRAF V600E inhibitor vemurafenib provides therapeutic benefits but the common emergence of drug resistance remains a challenge. To define molecular mechanisms of vemurafenib resistance, we generated A375-R, WM35-R cell lines resistant to vemurafenib and show that the phosphorylated (p)-STAT3 was upregulated in these cells in vitro and in vivo. In particular, activation of the Signal-transducer-and-activator-of-transcription 3 (STAT3) pathway was associated with vemurafenib resistance. Inhibition of this pathway with STAT3-specific siRNA (shRNA) sensitized A375-R, WM35-R cells to vemurafenib and induced apoptosis in vitro and in vivo. Moreover, targeting STAT3 induced expression of miR-579-3p and elicited resistance to vemurafenib. However, targeting microRNA (miR)-579-3p with anti-miR-579-3p reversed the resistance to vemurafenib. Together, these results indicated that STAT3-mediated downexpression of miR-579-3p caused resistance to vemurafenib. Our findings suggest novel approaches to overcome resistance to vemurafenib by combining vemurafenib with STAT3 sliencing or miR-579-3p overexpression.
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Registered trials
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