ArticleInternational journal of cancer2009
Caffeic acid phenethyl ester decreases cholangiocarcinoma growth by inhibition of NF-kappaB and induction of apoptosis.
Article in International journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 89 citations in OpenAlex.
- Digital Twin Meets the Bench: Natural Compounds Reshape the Ovarian Cancer Microenvironment.Biomedicines · 2025Article
- Melanoma cell adhesion molecule-positive mesenchymal stromal cells alleviate acute respiratory distress syndromeWorld journal of stem cells · 2025Article
- Caffeic Acid Phenethyl Ester: A Potential Therapeutic Cancer Agent?Current medicinal chemistry · 2024Review
- Oxidative Stress and Redox-Dependent Pathways in Cholangiocarcinoma.Antioxidants (Basel, Switzerland) · 2023Review
- Combination of Caffeic Acid Phenethyl Ester and Crocin Realign Potential Molecular Markers in U87-MG Glioma Cells.Current therapeutic research, clinical and experimental · 2023Article
- A Nano-Liposomal Formulation of Caffeic Acid Phenethyl Ester Modulates Nrf2 and NF-κβ Signaling and Alleviates Experimentally Induced Acute Pancreatitis in a Rat Model.Antioxidants (Basel, Switzerland) · 2022Article
- Article
- Propolis Extract and Its Bioactive Compounds-From Traditional to Modern Extraction Technologies.Molecules (Basel, Switzerland) · 2021Review
- Effects of caffeic acid on epigenetics in the brain of rats with chronic unpredictable mild stress.Molecular medicine reports · 2020Article
- An Update on the Role of Dietary Phytochemicals in Human Skin Cancer: New Insights into Molecular Mechanisms.Antioxidants (Basel, Switzerland) · 2020Review
- The Interaction Between lncRNA SNHG1 and miR-140 in Regulating Growth and Tumorigenesis via the TLR4/NF-κB Pathway in Cholangiocarcinoma.Oncology research · 2019Article
- The role of tumour microenvironment: a new vision for cholangiocarcinoma.Journal of cellular and molecular medicine · 2019Review
- Caffeic Acid Versus Caffeic Acid Phenethyl Ester in the Treatment of Breast Cancer MCF-7 Cells: Migration Rate Inhibition.Integrative cancer therapies · 2018Article
- Phytochemicals in Skin Cancer Prevention and Treatment: An Updated Review.International journal of molecular sciences · 2018Review
- Propolis and Its Potential to Treat Gastrointestinal Disorders.Evidence-based complementary and alternative medicine : eCAM · 2018Review
- Migration Rate Inhibition of Breast Cancer Cells Treated by Caffeic Acid and Caffeic Acid Phenethyl Ester: An In Vitro Comparison Study.Nutrients · 2017Article
- Comparison of Two Components of Propolis: Caffeic Acid (CA) and Caffeic Acid Phenethyl Ester (CAPE) Induce Apoptosis and Cell Cycle Arrest of Breast Cancer Cells MDA-MB-231.Molecules (Basel, Switzerland) · 2017Article
- Anti-colon cancer effect of caffeic acid p-nitro-phenethyl ester in vitro and in vivo and detection of its metabolites.Scientific reports · 2017Article
- An overview on the role of dietary phenolics for the treatment of cancers.Nutrition journal · 2016Review
- Capparis Spinosa L. promotes anti-inflammatory response in vitro through the control of cytokine gene expression in human peripheral blood mononuclear cells.BMC immunology · 2016Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Caffeic acid phenethyl ester (CAPE) inhibits the growth of tumor cells and is a known inhibitor of nuclear factor kappa beta (NF-kappaB), which is constitutively active in cholangiocarcinoma (CCH) cells. We evaluated the effects of CAPE on CCH growth both in vitro and in vivo. Inhibition of NF-kappaB DNA-binding activity was confirmed in nuclear extracts treated with CAPE at 50, 40 and 20 microM. CAPE decreases the expression of NF-kappaB1 (p50) and RelA (p65). CAPE decreased the growth of a number of CCH cells but not normal cholangiocytes. Cell cycle decrease was seen by a decrease in PCNA protein expression and the number of BrdU-positive cells treated with CAPE at 20 microM compared to vehicle. Inhibition of growth and increased cell cycle arrest of Mz-ChA-1 cells by CAPE were coupled with increased apoptosis. Bax expression was increased, whereas Bcl-2 was decreased in cells treated with CAPE compared to vehicle. In vivo studies were performed in BALB/c nude (nu/nu) mice implanted subcutaneously with Mz-ChA-1 cells and treated with daily IP injections of DMSO or CAPE (10 mg/kg body weight in DMSO) for 77 days. Tumor growth was decreased and tumor latency was increased 2-fold in CAPE compared to vehicle-treated nude mice. In tumor samples, decreased CCH growth by CAPE was coupled with increased apoptosis. CAPE both in vivo and in vitro decreases the growth of CCH cells by increasing apoptosis. These results demonstrate that CAPE might be an important therapeutic tool in the treatment of CCH.
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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.