ArticleFEBS open bio2018
Dasatinib promotes TRAIL-mediated apoptosis by upregulating CHOP-dependent death receptor 5 in gastric cancer.
Article in FEBS open bio, 2018. 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 It has been retracted, and should not be counted.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 12 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
12 citing papers in PubMed, 17 citations in OpenAlex.
- Molecular and Biochemical Evidence of Edaravone's Impact on Dasatinib-induced AGS Cell Senescence: A Promising Strategy for Gastric Cancer Therapy.Current medicinal chemistry · 2026Article
- Integrative machine learning reveals the biological function and prognostic significance of α-ketoglutarate in gastric cancer.Oncology letters · 2025Article
- Design and investigation of interactions of novel peptide conjugates of purine and pyrimidine derivatives with EGFR and its mutant T790M/L858R: an in silico and laboratory study.Molecular diversity · 2024Article
- Exploration of the link between COVID-19 and gastric cancer from the perspective of bioinformatics and systems biology.Frontiers in medicine · 2024Article
- Retraction statement: Luo L, Liu H and Xi Q (2018) Trastuzumab induces PUMA-dependent apoptosis and inhibits tumor growth in gastric cancer. FEBS Open Bio 8, 1911-1919.FEBS open bio · 2023Article
- AF8c, a Multi-Kinase Inhibitor Induces Apoptosis by Activating DR5/Nrf2 via ROS in Colorectal Cancer Cells.Cancers · 2022Article
- Mitochondrial dysfunction, UPRCell & bioscience · 2021Review
- Dasatinib prevents skeletal metastasis of osteotropic MDA-MB-231 cells in a xenograft mouse model.Archives of gynecology and obstetrics · 2020Article
- Identification of molecular targets for the targeted treatment of gastric cancer using dasatinib.Oncotarget · 2020Article
- Sodium fluoride induces apoptosis and autophagy via the endoplasmic reticulum stress pathway in MC3T3-E1 osteoblastic cells.Molecular and cellular biochemistry · 2019Article
- Dasatinib can enhance paclitaxel and gemcitabine inhibitory activity in human pancreatic cancer cells.Cancer biology & therapy · 2019Article
- TRAIL stabilization and cancer cell sensitization to its pro-apoptotic activity achieved through genetic fusion with arginine deiminase.Oncotarget · 2018Article
Corrections and comments
- Retraction · 2023-03-17Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Plagiarism of Image · Unreliable Results and/or Conclusions ·
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dasatinib, a tyrosine kinase inhibitor, has been approved for first-line treatment of leukemia and has also been evaluated for use in numerous other cancers. However, its role in gastric cancer (GC) remains unclear. Therefore, the aim of this study was to investigate how dasatinib suppresses the growth of GC cells and interacts with chemotherapeutic drugs. The results showed that, in the presence of dasatinib, proliferation of GC cells decreased and apoptosis increased, and that Fas-associated death domain protein and caspase-8 are essential to dasatinib-induced cell apoptosis in GC. In addition, we found that dasatinib increased the expression of death receptor 5 (DR5) in GC cells. Dasatinib enhanced apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in GC cells. Moreover, increased DR5 expression facilitated dasatinib-induced apoptosis; the dasatinib-induced increase in DR5 expression was mediated by CCAAT/enhancer-binding protein homologous protein (CHOP). Furthermore, dasatinib also synergized with TRAIL to induce apoptosis via DR5 in GC cells. Our results show that dasatinib promoted TRAIL-mediated apoptosis via upregulation of CHOP-dependent DR5 expression in GC, suggesting that DR5 induction can be used as an indicator of dasatinib sensitivity.
Indexed as
Identifiers
What OpenQuestion holds
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.