ArticleActa pharmacologica Sinica2015
Physalin B not only inhibits the ubiquitin-proteasome pathway but also induces incomplete autophagic response in human colon cancer cells in vitro.
Article in Acta pharmacologica Sinica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 31 citations in OpenAlex.
- Physalis minima L.: A comprehensive review on phytochemistry, pharmacology, and food applications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Inhibitory Effect of Alnustone on Survival and Lung Metastasis of Colorectal Cancer Cells.Nutrients · 2024Article
- Article
- Natural Products fromMolecules (Basel, Switzerland) · 2022Review
- Therapeutic Applications of Physalins: Powerful Natural Weapons.Frontiers in pharmacology · 2022Review
- Engineering ofBiomolecules · 2021Article
- ERK: A Double-Edged Sword in Cancer. ERK-Dependent Apoptosis as a Potential Therapeutic Strategy for Cancer.Cells · 2021Review
- Autophagy is a double-edged sword in the therapy of colorectal cancer.Oncology letters · 2021Review
- The Role of Oxidative Stress and Its Counteractive Utility in Colorectal Cancer (CRC).Cancers · 2020Review
- Anticancer activities of phytoconstituents and their liposomal targeting strategies against tumor cells and the microenvironment.Advanced drug delivery reviews · 2020Review
- Apoptotic Pathway as the Therapeutic Target for Anticancer Traditional Chinese Medicines.Frontiers in pharmacology · 2019Review
- Stereo- and region-specific biotransformation of physapubescin by four fungal strains.Journal of natural medicines · 2017Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the effects of physalin B insolated from Physalis divericata on human colon cancer cells in vitro and its anticancer mechanisms.
methodsHuman HCT116 colon cancer cell line was tested. Cell viability and apoptosis were detected, and relevant proteins were measured using Western blot analyses. Autophagosomes were observed in stable GFP-LC3 HCT116 cells. Localization of autophagosomes and lysosomes was evaluated in GFP-LC3/RFP-LAMP1-co-transfected cells. Microtubules and F-actin microfilaments were observed with confocal microscope. Mitochondrial ROS (mito-ROS) was detected with flow cytometry in the cells stained with MitoSox dye.
resultsPhysalin B inhibited the viability of HCT116 cells with an IC50 value of 1.35 μmol/L. Treatment of the cells with physalin B (2.5-10 μmol/L) induced apoptosis and the cleavage of PARP and caspase-3. Meanwhile, physalin B treatment induced autophagosome formation, and accumulation of LC3-II and p62, but decreased Beclin 1 protein level. Marked changes of microtubules and F-actin microfilaments were observed in physalin B-treated cells, which led to the blockage of co-localization of autophagosomes and lysosomes. Physalin B treatment dose-dependently increased the phosphorylation of p38, ERK and JNK in the cells, whereas the p38 inhibitor SB202190, ERK inhibitor U0126 or JNK inhibitor SP600125 could partially reduce physalin B-induced PARP cleavage and p62 accumulation. Moreover, physalin B treatment dose-dependently increased mito-ROS production in the cells, whereas the ROS scavenger NAC could reverse physalin B-induced effects, including incomplete autophagic response, accumulation of ubiquitinated proteins, changes of microtubules and F-actin, activation of p38, ERK and JNK, as well as cell death and apoptosis.
conclusionPhysalin B induces mito-ROS, which not only inhibits the ubiquitin-proteasome pathway but also induces incomplete autophagic response in HCT116 cells in vitro.
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