ArticleOxidative medicine and cellular longevity2019
DpdtbA-Induced Growth Inhibition in Human Esophageal Cancer Cells Involved Inactivation of the p53/EGFR/AKT Pathway.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- The oral microbiome and oral and upper gastrointestinal diseases.Journal of oral microbiology · 2024Review
- Systems biology and OMIC data integration to understand gastrointestinal cancers.World journal of clinical oncology · 2022Review
- Ferritinophagy-Mediated Ferroptosis and Activation of Keap1/Nrf2/HO-1 Pathway Were Conducive to EMT Inhibition of Gastric Cancer Cells in Action of 2,2'-Di-pyridineketone Hydrazone Dithiocarbamate Butyric Acid Ester.Oxidative medicine and cellular longevity · 2022Article
- Blockade of TRIM59 enhances esophageal cancer cell chemosensitivity to cisplatin by upregulating p53.Oncology letters · 2021Article
- Ferritinophagy-Mediated ROS Production Contributed to Proliferation Inhibition, Apoptosis, and Ferroptosis Induction in Action of Mechanism of 2-Pyridylhydrazone Dithiocarbamate Acetate.Oxidative medicine and cellular longevity · 2021Article
- ROS-Mediated Therapeutic Strategy in Chemo-/Radiotherapy of Head and Neck Cancer.Oxidative medicine and cellular longevity · 2020Review
- p53-R273H promotes cancer cell migration via upregulation of neuraminidase-1.Journal of Cancer · 2020Article
- Oxidative Stress-Induced circHBEGF Promotes Extracellular Matrix Production via Regulating miR-646/EGFR in Human Trabecular Meshwork Cells.Oxidative medicine and cellular longevity · 2020Article
- DpdtC-Induced EMT Inhibition in MGC-803 Cells Was Partly through Ferritinophagy-Mediated ROS/p53 Pathway.Oxidative medicine and cellular longevity · 2020Article
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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
Esophageal cancer (ESC) is one of the most deadly diseases for human. p53 in most cancers, including ESC cell, is mutated, and the mutated p53 losses its original function and acquires "gain of function" that allows for promoting the hallmarks of cancer, such as antiapoptosis, metastasis, invasion, angiogenesis, and resistance to chemotherapy. Targeting p53 through either introducing wild-type or degrading mutated p53 is an important strategy in cancer therapy. Di-2,2'-pyridine ketone dithiocarbamate s-butyric acid (DpdtbA) has significant growth inhibition against gastric cancer lines in previous study. Similar action in ESC cell lines but a novel molecular mechanism was observed in the present study. The results showed that DpdtbA exhibited an excellent antiproliferative effect for ESC cell lines (IC
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