ArticleNaunyn-Schmiedeberg's archives of pharmacology2019
Cucurbitacin B induces mitochondrial-mediated apoptosis pathway in cholangiocarcinoma cells via suppressing focal adhesion kinase signaling.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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
10 citing papers in PubMed, 20 citations in OpenAlex.
- Recent Advances in the Application of Cucurbitacin B as an Anticancer Agent.International journal of molecular sciences · 2025Review
- Research Progress of Chinese Medicine Monomers in Treatment of Cholangiocarcinoma.Chinese journal of integrative medicine · 2025Review
- Cucurbitacin B induces apoptosis in colorectal cells through reactive oxygen species generation and endoplasmic reticulum stress pathways.Experimental and therapeutic medicine · 2023Article
- Fruit Extract ofNutrients · 2023Article
- Modulation of Cytoskeleton, Protein Trafficking, and Signaling Pathways by Metabolites fromPharmaceuticals (Basel, Switzerland) · 2022Review
- Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit beta as a potential biomarker forParasitology · 2022Article
- Cucurbitacin B Diminishes Metastatic Behavior of Cholangiocarcinoma Cells by Suppressing Focal Adhesion Kinase.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- β-Eudesmol induces the expression of apoptosis pathway proteins in cholangiocarcinoma cell lines.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2020Article
- Inhibition of growth and migration of cholangiocarcinoma cells by pamidronate.Experimental and therapeutic medicine · 2019Article
- Unveiling the Anticancer Potential and Molecular Mechanisms of Fangchinoline Against Cholangiocarcinoma Using FTIR Microspectroscopy, In Vitro and In Silico Approaches.Integrative cancer therapiesArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Low efficacy and high resistance rate associated with existing chemotherapeutic drugs enforce a requirement for novel therapeutic strategies for extremely aggressive cholangiocarcinoma (CCA). In the present study, the apoptosis-inducing activity of cucurbitacin B, a compound derived from plants of Cucurbitaceae family, against KKU-100 CCA cells and the underlying mechanism mediating its effect were investigated. The results showed that cucurbitacin B significantly decreased CCA cells viability by induction of apoptosis. Increased apoptotic cell death following cucurbitacin B treatment was correlated with caspase-9 and caspase-3 activations, Bax upregulation, increased cytochrome c, apoptosis-inducing factor release, and decreased Bcl-2 and Bcl-XL levels, suggesting activation of the mitochondrial-mediated apoptosis pathway. Further molecular analyses revealed that cucurbitacin B inhibited focal adhesion kinase (FAK), which is an important regulator of the apoptosis process, and its downstream pathway, PI3K/Akt. Knockdown of FAK expression by small interfering RNA appeared to induce CCA cell apoptosis which was accompanied with elevated level of cytochrome c and cleaved caspase-9, and decreased level of Bcl-2, phospho-PI3K, and phospho-Akt. Taken together, cucurbitacin B induces an intrinsic mitochondrial apoptosis pathway in CCA cells partly through suppression of FAK-mediated oncogenic signaling. This compound should be considered as a candidate agent for CCA treatment.
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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 Socratic graph.