ArticleMolecular cancer research : MCR2021
Autophagy-Dependent Sensitization of Triple-Negative Breast Cancer Models to Topoisomerase II Poisons by Inhibition of the Nucleosome Remodeling Factor.
Article in Molecular cancer research : MCR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Loss of BPTF restores estrogen response and suppresses metastasis of mammary tumors.Nature communications · 2025Article
- Targeting the PI3K Pathway: Advancements and Achievements in Breast Cancer Therapy.Current pharmaceutical design · 2025Review
- A BPTF Inhibitor That Interferes with the Multidrug Resistance Pump to Sensitize Murine Triple-Negative Breast Cancer Cells to Chemotherapy.International journal of molecular sciences · 2024Article
- Bromodomain inhibition targeting BPTF in the treatment of melanoma and other solid tumors.Clinical & experimental metastasis · 2024Review
- Insights from a Computational-Based Approach for Analyzing Autophagy Genes across Human Cancers.Genes · 2023Review
- Design of Class I/IV Bromodomain-Targeting Degraders for Chromatin Remodeling Complexes.ACS chemical biology · 2023Article
- BPTF promotes the progression of distinct subtypes of breast cancer and is a therapeutic target.Frontiers in oncology · 2022Article
- New Design Rules for Developing Potent Cell-Active Inhibitors of the Nucleosome Remodeling Factor (NURF) via BPTF Bromodomain Inhibition.Journal of medicinal chemistry · 2021Article
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Epigenetic regulators can modulate the effects of cancer therapeutics. To further these observations, we discovered that the bromodomain PHD finger transcription factor subunit (BPTF) of the nucleosome remodeling factor (NURF) promotes resistance to doxorubicin, etoposide, and paclitaxel in the 4T1 breast tumor cell line. BPTF functions in promoting resistance to doxorubicin and etoposide, but not paclitaxel, and may be selective to cancer cells, as a similar effect was not observed in embryonic stem cells. Sensitization to doxorubicin and etoposide with BPTF knockdown (KD) was associated with increased DNA damage, topoisomerase II (TOP2) crosslinking and autophagy; however, there was only a modest increase in apoptosis and no increase in senescence. Sensitization to doxorubicin was confirmed
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Registered trials
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