ArticleCancer prevention research (Philadelphia, Pa.)2012
Caffeic acid phenethyl ester suppresses the proliferation of human prostate cancer cells through inhibition of p70S6K and Akt signaling networks.
Article in Cancer prevention research (Philadelphia, Pa.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Dietary polyphenols in prevention and treatment of prostate cancer.International journal of molecular sciences · 2015Pooled it
- A Mechanistic Digital Twin of uPAR-Driven Prostate Cancer Invasion Integrating ODE Signalling and Agent-Based Modelling.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Prostate cancer cells elevate glycolysis and G6PD in response to caffeic acid phenethyl ester-induced growth inhibition.BMC cancer · 2025Article
- Polyphenols: From Classification to Therapeutic Potential and Bioavailability.Foods (Basel, Switzerland) · 2024Review
- The miRNAs 203a/210-3p/5001-5p regulate the androgen/androgen receptor/YAP-induced migration in prostate cancer cells.Cancer medicine · 2024Article
- Plant phenolics inhibit focal adhesion kinase and suppress host cell invasion by uropathogenicInfection and immunity · 2024Article
- Efficacy of natural NF-κB inhibitors in the treatment of fibrosarcoma: an in vitro model study.Frontiers in cell and developmental biology · 2024Article
- Caffeic acid hinders the proliferation and migration through inhibition of IL-6 mediated JAK-STAT-3 signaling axis in human prostate cancer.Oncology research · 2024Article
- Development of a co-culture system for green production of caffeic acid from sugarcane bagasse hydrolysate.Frontiers in microbiology · 2024Article
- Caffeic Acid Phenethyl Ester (CAPE) Synergistically Enhances Paclitaxel Activity in Ovarian Cancer Cells.Molecules (Basel, Switzerland) · 2023Article
- Propolis: A Detailed Insight of Its Anticancer Molecular Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2023Review
- The Role of ERα and ERβ in Castration-Resistant Prostate Cancer and Current Therapeutic Approaches.Biomedicines · 2023Review
- Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15.Biomedical journal · 2022Article
- Molecular and Cellular Mechanisms of Propolis and Its Polyphenolic Compounds against Cancer.International journal of molecular sciences · 2022Review
- Combination treatment of docetaxel with caffeic acid phenethyl ester suppresses the survival and the proliferation of docetaxel-resistant prostate cancer cells via induction of apoptosis and metabolism interference.Journal of biomedical science · 2022Article
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- Caffeic acid phenethyl ester (CAPE) confers wild type p53 function in p53Discover oncology · 2021Article
- Recent progresses in the pharmacological activities of caffeic acid phenethyl ester.Naunyn-Schmiedeberg's archives of pharmacology · 2021Review
- The Pluripotent Activities of Caffeic Acid Phenethyl Ester.Molecules (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Caffeic acid phenethyl ester (CAPE) is a bioactive component derived from honeybee hive propolis. CAPE has been shown to have antimitogenic, anticarcinogenic, and other beneficial medicinal properties. Many of its effects have been shown to be mediated through its inhibition of NF-κB signaling pathways. We took a systematic approach to uncover the effects of CAPE from hours to days on the signaling networks in human prostate cancer cells. We observed that CAPE dosage dependently suppressed the proliferation of LNCaP, DU-145, and PC-3 human prostate cancer cells. Administration of CAPE by gavage significantly inhibited the tumor growth of LNCaP xenografts in nude mice. Using LNCaP cells as a model system, we examined the effect of CAPE on gene expression, protein signaling, and transcriptional regulatory networks using micro-Western arrays and PCR arrays. We built a model of the impact of CAPE on cell signaling which suggested that it acted through inhibition of Akt-related protein signaling networks. Overexpression of Akt1 or c-Myc, a downstream target of Akt signaling, significantly blocked the antiproliferative effects of CAPE. In summary, our results suggest that CAPE administration may be useful as an adjuvant therapy for prostate and potentially other types of cancers that are driven by the p70S6K and Akt signaling networks.
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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 OpenQuestion graph.