ArticleScientific reports2015
Tetrathiomolybdate mediates cisplatin-induced p38 signaling and EGFR degradation and enhances response to cisplatin therapy in gynecologic cancers.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Differential Effects of Mesenchymal Stem Cell- and Natural Killer Cell-Derived Extracellular Vesicles on Cisplatin Responsiveness in Endometrial Cancer Cells.International journal of molecular sciences · 2026Article
- Targeting cuproptosis for treatment and prognostic assessment in endometrial cancer.Cancer cell international · 2025Review
- Copper Dyshomeostasis and Diabetic Complications: Chelation Strategies for Management.Mini reviews in medicinal chemistry · 2025Review
- Cuproptosis-related genes and agents: implications in tumor drug resistance and future perspectives.Frontiers in pharmacology · 2025Review
- Copper in Gynecological Diseases.International journal of molecular sciences · 2023Review
- Article
- Ubiquitin chromatin remodelling after DNA damage is associated with the expression of key cancer genes and pathways.Cellular and molecular life sciences : CMLS · 2021Article
- Current Biomedical Use of Copper Chelation Therapy.International journal of molecular sciences · 2020Review
- Ammonium tetrathiomolybdate enhances the antitumor effect of cisplatin via the suppression of ATPase copper transporting beta in head and neck squamous cell carcinoma.Oncology reports · 2019Article
- Blockage of SLC31A1-dependent copper absorption increases pancreatic cancer cell autophagy to resist cell death.Cell proliferation · 2019Article
- Anticancer response to disulfiram may be enhanced by co-treatment with MEK inhibitor or oxaliplatin: modulation by tetrathiomolybdate, KRAS/BRAF mutations and c-MYC/p53 status.Ecancermedicalscience · 2019Article
- Mechanisms for DNA-damaging agent-induced inactivation of ErbB2 and ErbB3 via the ERK and p38 signaling pathways.Oncology letters · 2018Article
- Growth Hormone differentially modulates chemoresistance in human endometrial adenocarcinoma cell lines.Endocrine · 2017Article
- The Molecular Mechanisms of Regulation on USP2's Alternative Splicing and the Significance of Its Products.International journal of biological sciences · 2017Review
- Effect of the BRCA1-SIRT1-EGFR axis on cisplatin sensitivity in ovarian cancer.American journal of translational research · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Cisplatin and its analogs are among the most widely used chemotherapeutic agents against various types of cancer. It is known that cisplatin can activate epidermal growth factor receptor (EGFR), which may provide a survival benefit in cancers. Tetrathiomolybdate (TM) is a potent anti-cancer and anti-angiogenic agent and has been investigated in a number of clinical trials for cancer. In this study, we explore the therapeutic potential of TM on cisplatin-mediated EGFR regulation. Our study shows that TM is not cytotoxic, but exerts an anti-proliferative effect in ECC-1 cells. However, TM treatment prior to cisplatin markedly improves cisplatin-induced cytotoxicity. TM suppressed cisplatin-induced activation of EGFR while potentiating activation of p38; the activation of p38 signaling appeared to promote cisplatin-induced EGFR degradation. These results are in contrast to what we saw when cells were co-treated with cisplatin plus an EGFR tyrosine kinase inhibitor, where receptor activation was inhibited but receptor degradation was also blocked. Our current study is in agreement with previous findings that TM may have a therapeutic benefit by inhibiting EGFR activation. We furthermore provide evidence that TM may provide an additional benefit by potentiating p38 activation following cisplatin treatment, which may in turn promote receptor degradation by cisplatin.
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