ArticleOncoTargets and therapy2020
Emodin Reverses Gemcitabine Resistance of Pancreatic Cancer Cell Lines Through Inhibition of IKKβ/NF-κB Signaling Pathway.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Systematically investigate the mechanism underlying the therapeutic effect of emodin in treatment of prostate cancer.Discover oncology · 2025Article
- The LAMB3-EGFR signaling pathway mediates synergistic Anti-Cancer effects of berberine and emodin in Pancreatic cancer.Biochemical pharmacology · 2024Article
- Review
- Article
- IκB kinase β (IKKβ): Structure, transduction mechanism, biological function, and discovery of its inhibitors.International journal of biological sciences · 2023Review
- Advances in the pharmacological effects and molecular mechanisms of emodin in the treatment of metabolic diseases.Frontiers in pharmacology · 2023Review
- Advances in the treatment of pancreatic cancer with traditional Chinese medicine.Frontiers in pharmacology · 2023Review
- Emodin Ameliorates the Efficacy of Carfilzomib in Multiple Myeloma Cells via Apoptosis and Autophagy.Biomedicines · 2022Article
- Emodin exerts antitumor effects in ovarian cancer cell lines by preventing the development of cancer stem cells via epithelial mesenchymal transition.Oncology letters · 2022Article
- Platelet-Vesicles-Encapsulated RSL-3 Enable Anti-Angiogenesis and Induce Ferroptosis to Inhibit Pancreatic Cancer Progress.Frontiers in endocrinology · 2022Article
- The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers.International journal of biological sciences · 2022Review
- The Health Benefits of Emodin, a Natural Anthraquinone Derived from Rhubarb-A Summary Update.International journal of molecular sciences · 2021Review
- Cancer Chemoprevention: A Strategic Approach Using Phytochemicals.Frontiers in pharmacology · 2021Review
- Emodin Interferes With AKT1-Mediated DNA Damage and Decreases Resistance of Breast Cancer Cells to Doxorubicin.Frontiers in oncology · 2020Article
- Therapeutic Potential of Emodin for Gastrointestinal Cancers.Integrative cancer therapiesReview
- Emodin-induced cell cycle arrest: A promising approach for cancer therapy (Review).Medicine internationalReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPancreatic cancer is one of the most malignant tumors, and gemcitabine has been considered as the standard treatment and been widely utilized as a first-line drug for advanced pancreatic cancer, but gemcitabine-resistance always occurs after a short period of treatment.
methodsTwo pancreatic cancer cell lines Panc-1 and MIA-PaCa-2 were used as the study subject and their gemcitabine-resistant cells were established. Both drug-resistant cells were divided into four groups: blank, emodin, gemcitabine, and emodin+gemcitabine. Cell viability was detected by MTT assay. Flow cytometry was performed to detect cell apoptosis rate and P-gp function. Quantitative real-time polymerase chain reaction and Western blotting were used to detect
resultsEmodin could inhibit cell activity in all cell lines. Both emodin and gemcitabine can significantly increase the apoptosis rate, and the combination of the two drugs can further significantly increase the apoptosis rate in normal pancreatic cancer cell lines. In both drug-resistant pancreatic cancer cell lines, it can be observed that although gemcitabine can increase the apoptosis rate, the effect of promoting apoptosis is significantly lower than that of emodin; the drug combination can still significantly increase the apoptosis rate on the basis of emodin alone. Emodin can significantly reduce the mRNA and protein expression levels of
conclusionEmodin inhibits the expression of
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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.