ArticleJournal of cellular and molecular medicine2020
Chelerythrine induces apoptosis via ROS-mediated endoplasmic reticulum stress and STAT3 pathways in human renal cell carcinoma.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- A multifunctional 5-fluorouracil prodrug: synthesis, biological evaluation, and antitumor mechanism investigation.Molecular diversity · 2026Article
- Cypripedin Induces Apoptosis and Synergizes with Bortezomib via ER Stress Mediated Ubiquitination of GRP78 in T-Cell Acute Lymphoblastic Leukemia.Molecules (Basel, Switzerland) · 2026Article
- Chelerythrine-mediated targeting of NF-κB and Nrf2 pathways alleviates liver injury in a carbon tetrachloride-induced liver fibrosis mouse model.Histology and histopathology · 2025Article
- Chelerythrine inhibits esophageal squamous cell carcinoma progression via PINK1-Parkin-mediated mitophagy.Journal of translational medicine · 2025Article
- Anticancer Activity ofBiomolecules · 2025Article
- Review
- Elucidating the anticancer potential of dendrobine in renal cell carcinoma treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Tumour heterogeneity and personalized treatment screening based on single-cell transcriptomics.Computational and structural biotechnology journal · 2025Article
- Insights on Antitumor Activity and Mechanism of Natural Benzophenanthridine Alkaloids.Molecules (Basel, Switzerland) · 2023Review
- Article
- Endoplasmic Reticulum Stress in Renal Cell Carcinoma.International journal of molecular sciences · 2023Review
- SLC17A9-PTHLH-EMT axis promotes proliferation and invasion of clear renal cell carcinoma.iScience · 2023Article
- Isolation and identification of bioactive compounds from Antrodia camphorata against ESKAPE pathogens.PloS one · 2023Article
- Chelerythrine-Induced Apoptotic Cell Death in HepG2 Cells Involves the Inhibition of Akt Pathway and the Activation of Oxidative Stress and Mitochondrial Apoptotic Pathway.Antioxidants (Basel, Switzerland) · 2022Article
- Fluorescence, Absorption, Chromatography and Structural Transformation of Chelerythrine and Ethoxychelerythrine in Protic Solvents: A Comparative Study.Molecules (Basel, Switzerland) · 2022Article
- Review
- Therapeutic Potential of Natural Products in the Treatment of Renal Cell Carcinoma: A Review.Nutrients · 2022Review
- Sanguinarine-Chelerythrine Fraction ofOxidative medicine and cellular longevity · 2022Article
- Rediscovery of Traditional Plant Medicine: An Underestimated Anticancer Drug of Chelerythrine.Frontiers in pharmacology · 2022Review
- Fructose-1,6-bisphosphatase aggravates oxidative stress-induced apoptosis in asthma by suppressing the Nrf2 pathway.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal cell carcinoma (RCC) is a heterogeneous histological disease and it is one of the most common kidney cancer. The treatment of RCC has been improved for the past few years, but its mortality still remains high. Chelerythrine (CHE) is a natural benzo[c]phenanthridine alkaloid and a widely used broad-range protein kinase C inhibitor which has anti-cancer effect on various types of human cancer cells. However, its effect on RCC has not been fully elucidated. In this study, we evaluated the effect and mechanism of CHE on RCC cells. Our study showed that CHE induced colony formation inhibition and G2/M cell cycle arrest in a dose-dependent manner in RCC cells. In addition, CHE increased cellular ROS level, leading to endoplasmic reticulum (ER) stress, inactivating STAT3 activities and inducing apoptosis in RCC cells which were suppressed by NAC, a special ROS inhibitor. We further found that both knockdown of ATF4 protein and overexpression of STAT3 protein could reduce CHE-induced apoptosis in Caki cells. These results demonstrated that the apoptosis induced by CHE was mediated by ROS-caused ER stress and STAT3 inactivation. Collectively, our studies provided support for CHE as a potential new therapeutic agent for the management of RCC.
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