ArticleThe Journal of investigative dermatology2013
Stat3-targeted therapies overcome the acquired resistance to vemurafenib in melanomas.
Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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59 citing papers in PubMed, 109 citations in OpenAlex.
- Polyamine and EIF5A hypusination downstream of c-Myc confers targeted therapy resistance in BRAF mutant melanoma.Molecular cancer · 2024Article
- Alantolactone enhances the sensitivity of melanoma to MAPK pathway inhibitors by targeting inhibition of STAT3 activation and down-regulating stem cell markers.Cancer cell international · 2024Article
- Molecular network mechanism of Shexiang Huayu Xingnao granules in treating intracerebral hemorrhage.Ibrain · 2024Article
- Enhancing immunotherapy response in melanoma: myeloid-derived suppressor cells as a therapeutic target.The Journal of clinical investigation · 2023Review
- Overcoming Acquired Drug Resistance to Cancer Therapies through Targeted STAT3 Inhibition.International journal of molecular sciences · 2023Review
- Role of IL-6/STAT3 Axis in Resistance to Cisplatin in Gastric Cancers.Biomedicines · 2023Article
- Efficient prioritization of CRISPR screen hits by accounting for targeting efficiency of guide RNA.BMC biology · 2023Article
- Combination of a STAT3 inhibitor with anti-PD-1 immunotherapy is an effective treatment regimen for a vemurafenib-resistant melanoma.Molecular therapy oncolytics · 2022Article
- The effect of local non-thermal plasma therapy on the cancer-immunity cycle in a melanoma mouse model.Bioengineering & translational medicine · 2022Article
- Combined MEK and JAK/STAT3 pathway inhibition effectively decreases SHH medulloblastoma tumor progression.Communications biology · 2022Article
- Potential Biomarkers of Skin Melanoma Resistance to Targeted Therapy-Present State and Perspectives.Cancers · 2022Review
- Early differential responses elicited by BRAFCell death & disease · 2022Article
- Hinokiflavone Inhibits Growth of Esophageal Squamous Cancer By Inducing ApoptosisFrontiers in oncology · 2022Article
- Chemoreversal Agents from Taiwanofungus Genus and Their More Potent Methyl Derivatives Targeting Signal Transducer and Activator of Transcription 3 (STAT3) Phosphorylation.Pharmaceuticals (Basel, Switzerland) · 2021Article
- HER3-Receptor-Mediated STAT3 Activation Plays a Central Role in Adaptive Resistance toward Vemurafenib in Melanoma.Cancers · 2020Article
- Formulation of Stattic as STAT3 inhibitor in nanostructured lipid carriers (NLCs) enhances efficacy of doxorubicin in melanoma cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- SilencingAging · 2020Article
- Dual Inhibition of MAPK and JAK2/STAT3 Pathways Is Critical for the Treatment of BRAF Mutant Melanoma.Molecular therapy oncolytics · 2020Article
- Article
- Balancing STAT Activity as a Therapeutic Strategy.Cancers · 2019Review
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9 authors at 4 institutions in 2 countries.
Funding
Abstract
Vemurafenib (PLX4032), a selective inhibitor of Braf, has been approved by the US Food and Drug Administration for the treatment of unresectable or metastatic melanoma in patients with Braf(V600E) mutations. Many patients treated with vemurafenib initially display dramatic improvement, with decreases in both risk of death and tumor progression. Acquired resistance, however, rapidly arises in previously sensitive cells. We attempted to overcome this resistance by targeting the signal transducer and activator of transcription 3 (STAT3)-paired box homeotic gene 3 (PAX3)-signaling pathway, which is upregulated, owing to fibroblast growth factor 2 (FGF2) secretion or increased kinase activity, with the Braf(V600E) mutation. We found that activation of Stat3 or overexpression of PAX3 induced resistance to vemurafenib in melanoma cells. In addition, PAX3 or Stat3 silencing inhibited the growth of melanoma cells with acquired resistance to vemurafenib. Furthermore, treatment with the Stat3 inhibitor, WP1066, resulted in growth inhibition in both vemurafenib-sensitive and -resistant melanoma cells. Significantly, vemurafenib stimulation induced FGF2 secretion from keratinocytes and fibroblasts, which might uncover, at least in part, the mechanisms underlying targeting Stat3-PAX3 signaling to overcome the acquired resistance to vemurafenib. Our results suggest that Stat3-targeted therapy is a new therapeutic strategy to overcome the acquired resistance to vemurafenib in the treatment of melanoma.
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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.