ArticleAmerican journal of cancer research2020
FBP1 binds to the bromodomain of BRD4 to inhibit pancreatic cancer progression.
Article in American journal of cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Metabolic Regulation of Immune Responses: Molecular Mechanisms, Diseases, and Therapeutic Targets.MedComm · 2026Review
- MLN4924 suppresses tumor metabolism and growth of clear cell renal cell carcinoma by stabilizing nuclear FBP1.Cell death discovery · 2025Article
- The role of fructose-1,6-bisphosphatase 1 on regulating the cancer progression and drug resistance.Discover oncology · 2025Review
- WDR3 drives pancreatic cancer metastasis by enhancing TGF-α mRNA stability through YTHDC1.American journal of cancer research · 2025Article
- FBP1 is a potential prognostic biomarker and correlated with tumor immunosuppressive microenvironment in glioblastoma.Neurosurgical review · 2023Article
- Metformin acts in the gut and induces gut-liver crosstalk.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Heat Shock Transcription Factor 2 Is Significantly Involved in Neurodegenerative Diseases, Inflammatory Bowel Disease, Cancer, Male Infertility, and Fetal Alcohol Spectrum Disorder: The Novel Mechanisms of Several Severe Diseases.International journal of molecular sciences · 2022Review
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- Andrographolide inhibits non-small cell lung cancer cell proliferation through the activation of the mitochondrial apoptosis pathway and by reprogramming host glucose metabolism.Annals of translational medicine · 2021Article
- Overcoming chemoresistance by targeting reprogrammed metabolism: the Achilles' heel of pancreatic ductal adenocarcinoma.Cellular and molecular life sciences : CMLS · 2021Review
- Fructose-1,6-bisphosphatase aggravates oxidative stress-induced apoptosis in asthma by suppressing the Nrf2 pathway.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive tumour that is characteristically unresponsive to most chemotherapeutic regimens. Bromodomain and extra terminal domain (BET) inhibitors that specifically repress the function of BET family proteins, such as BRD4, are under evaluation in clinical trials for their activity in repressing cancer growth. However, resistance to BET inhibitors has hindered their further clinical application in pancreatic cancer. We previously reported that FBP1 contributes to the resistance to BET inhibitors, but the underlying mechanism of this resistance remains unclear. Herein, we demonstrate that FBP1 is a binding partner of BRD4 in pancreatic cancer cells. We reveal that FBP1 binds to the BD2 domain of BD4 in an acetylation-dependent manner. Moreover, we found that Tip60 and HDAC3 were key to the acetylation and de-acetylation of FBP1 at K110 and K113, which are critical for mediating FBP1-BRD4 binding in pancreatic cancer cells. Furthermore, our data indicate that FBP1 decreases the expression of genes downstream of BRD4 to inhibit pancreatic cancer cell progression. Our results, therefore, provide evidence of the novel anti-tumour effect of FBP1 via its blockade of BRD4 function in pancreatic cancer cells.
Indexed as
Identifiers
32195024PMC7061763What OpenQuestion holds
Registered trials
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