ArticleAmerican journal of cancer research2021
Hyperphosphorylation of HDAC2 promotes drug resistance in a novel dual drug resistant mouse melanoma cell line model: an
Article in American journal of cancer research, 2021. 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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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Quinoline conjugates for enhanced antimalarial activity: a review on synthesis by molecular hybridization and structure-activity relationship (SAR) investigation.American journal of translational research · 2025Review
- HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023Review
- Efficacy of 15% lysine cream in treating diabetic foot ulcers: a randomized interventional study.International journal of physiology, pathophysiology and pharmacology · 2023Article
- The paradigm of drug resistance in cancer: an epigenetic perspective.Bioscience reports · 2022Review
- Characterization of antidepressant activity ofAmerican journal of translational research · 2022Article
- Bowman's membrane lenticule tuck-in: A new approach for the management of neurotrophic ulcers.Saudi journal of ophthalmology : official journal of the Saudi Ophthalmological SocietyArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug-resistant melanoma is very difficult to treat, and a novel approach is needed to overcome resistance. The present study aims at identifying the alternate pathways utilized in the dual drug-resistant mouse melanoma cells (B16F10R) for their survival and proliferation. The dual drug-resistant mouse melanoma, B16F10R, was established by treating the cells with a combination of U0126 (MEK1/2 inhibitor) and LY294002 (PI3K-AKT kinase inhibitor) in a dose-escalating manner till they attained a resistance fold factor of ≥2. The altered phosphoproteome in the B16F10R, as compared to the parental B16F10C, was analyzed using a high-resolution Orbitrap Fusion Tribrid mass spectrometer. Histone deacetylases 2 (HDAC2) was validated for its role in drug resistance by using its inhibitor, valproic acid (VPA). In the B16F10R cells, 363 altered phosphoproteins were identified, among which 126 were hyperphosphorylated, and 137 were hypophosphorylated (1.5-fold change). Pathway analysis shows the altered phosphoproteins are from RNA metabolism and cell cycle proteins. Inhibition of HDAC2 by VPA induces apoptosis in B16F10C and B16F10R. The present study highlights the role of HDAC2, a cell cycle regulator, in the development of resistance to dual drugs in murine melanoma. Therefore, designing leads for targeting HDAC2 along with key signaling pathways may be explored in treatment strategies.
Indexed as
Identifiers
35018231PMC8727796W4206878169What Socratic 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 Socratic graph.