ArticleJournal of experimental & clinical cancer research : CR2019
PES1 promotes BET inhibitors resistance and cells proliferation through increasing c-Myc expression in pancreatic cancer.
Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- ELF3-regulated PES1 targets VEGFR2 to mediate angiogenesis and retinal inner barrier injury in diabetic retinopathy.Journal of translational medicine · 2025Article
- Pescadillo ribosomal biogenesis factor 1 as a therapeutic target in tumor immunotherapy.World journal of gastroenterology · 2025Article
- mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Immunotherapy resistance in solid tumors: mechanisms and potential solutions.Cancer biology & therapy · 2024Review
- Targeting CBX3 with a Dual BET/PLK1 Inhibitor Enhances the Antitumor Efficacy of CDK4/6 Inhibitors in Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Glutamine addiction and therapeutic strategies in pancreatic cancer.World journal of gastrointestinal oncology · 2023Review
- The SUMOylation and ubiquitination crosstalk in cancer.Journal of cancer research and clinical oncology · 2023Review
- PES1 is a biomarker of head and neck squamous cell carcinoma and is associated with the tumor microenvironment.Cancer medicine · 2023Article
- PES1 reduces CD8Journal of biomedical science · 2023Article
- Pescadillo ribosomal biogenesis factor 1 reduction suppresses tumour growth and renders chemosensitivity of head and neck squamous cell carcinoma.Cancer medicine · 2023Article
- Anti‑silencing function 1B promotes the progression of pancreatic cancer by activating c‑Myc.International journal of oncology · 2023Article
- Target c-Myc to treat pancreatic cancer.Cancer biology & therapy · 2022Article
- PROTACs in gastrointestinal cancers.Molecular therapy oncolytics · 2022Review
- The RBPJ/DAPK3/UBE3A signaling axis induces PBRM1 degradation to modulate the sensitivity of renal cell carcinoma to CDK4/6 inhibitors.Cell death & disease · 2022Article
- Long non-coding RNA DSCAM-AS1 promotes pancreatic cancer progression via regulating the miR-136-5p/PBX3 axis.Bioengineered · 2022Article
- Bromodomain and extra-terminal inhibitors emerge as potential therapeutic avenues for gastrointestinal cancers.World journal of gastrointestinal oncology · 2022Review
- The functional role of Pescadillo ribosomal biogenesis factor 1 in cancer.Journal of Cancer · 2022Review
- Establish of an Initial Platinum-Resistance Predictor in High-Grade Serous Ovarian Cancer Patients Regardless of Homologous Recombination Deficiency Status.Frontiers in oncology · 2022Article
- SNHG17 promotes colorectal tumorigenesis and metastasis via regulating Trim23-PES1 axis and miR-339-5p-FOSL2-SNHG17 positive feedback loop.Journal of experimental & clinical cancer research : CR · 2021Article
- MIB1 upregulates IQGAP1 and promotes pancreatic cancer progression by inducing ST7 degradation.Molecular oncology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundOverexpressed PES1 promotes carcinogenesis in various types of malignant tumors. However, the biological role and clinical significance of PES1 in pancreatic cancer are still unexplored.
methodsThe expression level of PES1 in pancreatic cancer cell lines and pancreatic cancer patient samples was determined using Western Blotting analysis, RT-qPCR analysis, immunohistochemical (IHC) analysis of tissue microarray, and the GEPIA web tool. MTS assay, colony formation assay, and xenograft tumor assay were used to evaluate the tumor growth ability of pancreatic cancer cells.
resultsWe established that the expression of PES1 was abnormally increased in pancreatic cancer tissues and led to poor prognosis of pancreatic cancer patients. We also found that PES1 was responsible for promoting cell growth and contributed to bromodomain and cancer cell resistance to extra-terminal (BET) inhibitors in pancreatic cancer. Furthermore, we showed that PES1 interacted with BRD4 to enhance c-Myc expression, which is the primary cause of cancer cell resistance to BET inhibitors in pancreatic cancer. Finally, CDK5 inhibitors were proven to destabilize PES1 and overcome cancer cell resistance to BET inhibitors in pancreatic cancer cells.
conclusionsWe have shown that PES1 could be one of the promoting factors of tumor growth and a prognosis-related protein of pancreatic cancer. Targeting PES1 with CDK5 inhibitors might help overcome cancer cell resistance to BET inhibitors in pancreatic cancer cells.
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