ArticleJournal of cellular and molecular medicine2022
Mcl-1 inhibition overcomes BET inhibitor resistance induced by low FBW7 expression in breast cancer.
Article in Journal of cellular and molecular medicine, 2022. 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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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Recommended Tool Compounds: Thienotriazolodiazepines-Derivatized Chemical Probes to Target BET Bromodomains.ACS pharmacology & translational science · 2025Review
- Ubiquitination and deubiquitination in cancer: from mechanisms to novel therapeutic approaches.Molecular cancer · 2024Review
- Capivasertib reverses chemotherapy-induced esophageal cancer resistance via inhibiting Akt-associated Mcl-1 upregulation.Heliyon · 2024Article
- FBXW7 in breast cancer: mechanism of action and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2023Review
- Mcl-1 inhibition overcomes BET inhibitor resistance induced by low FBW7 expression in breast cancer.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While the promise of bromodomains and extraterminal (BET) protein inhibitors (BETis) is emerging in breast cancer (BC) therapy, resistance in these cells to BETis conspicuously curbs their therapeutic potential. FBW7 is an important tumour suppressor. However, the role of FBW7 in BC is not clear. In the current study, our data indicated that the low expression of FBW7 contributes to the drug resistance of BC cells upon JQ1 treatment. shRNA-mediated FBW7 silencing in FBW7 WT BC cells suppressed JQ1-induced apoptosis. Mechanistically, it was revealed that this diminished FBW7 level leads to Mcl-1 stabilization, while Mcl-1 upregulation abrogates the killing effect of JQ1. Mcl-1 knockdown or inhibition resensitized the BC cells to JQ1-induced apoptosis. Moreover, FBW7 knockdown in MCF7 xenografted tumours demonstrated resistance to JQ1 treatment. The combination of JQ1 with a Mcl-1 inhibitor (S63845) resensitized the FBW7 knockdown tumours to JQ1 treatment in vivo. Our study paves the way for a novel therapeutic potential of BETis with Mcl-1 inhibitors for BC patients with a low FBW7 expression.
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