ArticlePloS one2013
Casticin potentiates TRAIL-induced apoptosis of gastric cancer cells through endoplasmic reticulum stress.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 54 citations in OpenAlex.
- Combination therapies and novel delivery systems: a new frontier in overcoming TRAIL resistance in gastric cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Alternative medicines in oncology: a focus on natural products against gastric cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Exploring natural products as apoptosis modulators in cancers: insights into natural product-based therapeutic strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Catechin promotes endoplasmic reticulum stress-mediated gastric cancer cell apoptosis via NOX4-induced reactive oxygen species.Molecular and cellular biochemistry · 2025Article
- Retraction: Casticin potentiates TRAIL-induced apoptosis of gastric cancer cells through endoplasmic reticulum stress.PloS one · 2025Article
- Flavonoids and Gastric Cancer Therapy: From Signaling Pathway to Therapeutic Significance.Drug design, development and therapy · 2024Review
- Casticin as potential anticancer agent: recent advancements in multi-mechanistic approaches.Frontiers in molecular biosciences · 2023Review
- New Visions on Natural Products and Cancer Therapy: Autophagy and Related Regulatory Pathways.Cancers · 2022Review
- Casticin inhibits esophageal cancer cell proliferation and promotes apoptosis by regulating mitochondrial apoptotic and JNK signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2019Article
- The Role of the ER-Induced UPR Pathway and the Efficacy of Its Inhibitors and Inducers in the Inhibition of Tumor Progression.Oxidative medicine and cellular longevity · 2019Review
- Flavonoids in Cancer and Apoptosis.Cancers · 2018Review
- Anti-Cancer Natural Products and Their Bioactive Compounds Inducing ER Stress-Mediated Apoptosis: A Review.Nutrients · 2018Review
- The regulation of combined treatment-induced cell death with recombinant TRAIL and bortezomib through TRAIL signaling in TRAIL-resistant cells.BMC cancer · 2018Article
- Casticin inhibits the epithelial-mesenchymal transition in ovarian carcinoma via the hedgehog signaling pathway.Oncology letters · 2018Article
- MDL-12330A potentiates TRAIL-induced apoptosis in gastric cancer cells through CHOP-mediated DR5 upregulation.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017Article
- Andrographolide induces apoptotic and non-apoptotic death and enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in gastric cancer cells.Oncology letters · 2017Article
- Casticin inhibits the activity of transcription factor Sp1 and the methylation ofExperimental and therapeutic medicine · 2017Article
- Casticin induces apoptosis and G0/G1 cell cycle arrest in gallbladder cancer cells.Cancer cell international · 2017Article
- A candidate Chinese medicine preparation-Fructus Viticis Total Flavonoids inhibits stem-like characteristics of lung cancer stem-like cells.BMC complementary and alternative medicine · 2016Article
- The alkyllysophospholipid edelfosine enhances TRAIL-mediated apoptosis in gastric cancer cells through death receptor 5 and the mitochondrial pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
Corrections and comments
- Retraction · 2025-04-15Author Unresponsive · Concerns/Issues about Image · Contamination of Cell Lines/Tissues · Duplication of/in Image · Euphemisms for Duplication · Original Data and/or Images not Provided and/or not Available · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCasticin is one of the main active components obtained from Fructus Viticis and has been reported to exert anti-carcinogenic activity on a variety of cancer cells but the precise mechanism underlying this activity remains unclear. MATERIALS AND
methodsApoptotic activities of casticin (1.0 µmol/l) and TRAIL (25, 50 ng/ml) alone or in combination in the gastric cancer cell lines BGC-823, SGC-7901 and MGC-803 were detected by the use of a cell apoptosis ELISA detection kit, flow cytometry (FCM) with propidium iodide (PI) staining and activities of caspase-3, -8 and -9 by ELISA and cleavage of polyADP-ribose polymerase (PARP) protein using western blot analysis. Death receptors (DR) expression levels were evaluated using FCM analysis and western blotting. 2', 7'-dichlorofluorescein diacetate (DCFH-DA) was used as a probe to measure the increase in reactive oxygen species (ROS) levels in cells. Multiple interventions, such as siRNA transfection and pharmacological inhibitors were used to explore the mechanisms of these actions.
resultsSubtoxic concentrations of casticin significantly potentiated TRAIL-induced cytotoxicity and apoptosis in BGC-823, SGC-7901 and MGC-803 cells. Casticin dramatically upregulated DR5 receptor expression but had no effects on DR4 or decoy receptors. Deletion of DR5 by siRNA significantly reduced the apoptosis induced by the co-application of TRAIL and casticin. Gene silencing of the CCAAT/enhancer binding protein homologous protein (CHOP) and pretreatment with salubrinal, an endoplasmic reticulum (ER) stress inhibitor, attenuated casticin-induced DR5 receptor expression, and apoptosis and ROS production. Casticin downregulated the expression levels of the cell survival proteins cFLIP, Bcl-2, XIAP, and survivin. In addition, casticin also induced the expressions of DR5 protein in other gastric cancer cells (SGC-7901 and MGC-803). CONCLUSION/SIGNIFICANCE: Casticin enhances TRAIL-induced apoptosis through the downregulation of cell survival proteins and the upregulation of DR5 receptors through actions on the ROS-ER stress-CHOP pathway.
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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.