ArticleCancer management and research2020
Pyrrolidine Dithiocarbamate Facilitates Arsenic Trioxide Against Pancreatic Cancer via Perturbing Ubiquitin-Proteasome Pathway.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- A Tumor Homing Peptide-Linked Arsenic Compound Inhibits Pancreatic Cancer Growth and Enhances the Inhibitory Effect of Gemcitabine.International journal of molecular sciences · 2024Article
- Trace elements in pancreatic cancer.Cancer medicine · 2024Review
- Arsenic trioxide: applications, mechanisms of action, toxicity and rescue strategies to date.Archives of pharmacal research · 2024Review
- Arsenic trioxide: applications, mechanisms of action, toxicity and rescue strategies to date.Archives of pharmacal research · 2024Review
- Application of Mass Spectrometry in Pancreatic Cancer Translational Research.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate whether pyrrolidine dithiocarbamate (PDTC) could facilitate arsenic trioxide (ATO) to induce apoptosis in pancreatic cancer cells via perturbing ubiquitin-proteasome pathway.
methodsMass spectrometry was performed to examine the interaction between PDTC and ATO, and the data showed they could form a complex termed PDTC-ATO. Inhibiting effects on cell viability were examined by CCK-8 test, and apoptosis was examined by flow cytometry. Four treatment arms (n = 6), including the control, PDTC, ATO, and PDTC-ATO, were evaluated using BALB/c nude mouse models bearing a xenograft tumor of SW1990 human pancreatic cancer line. Western blot, immunohistochemistry assays were to detect the mechanism.
resultsThe results showed that PDTC-ATO had higher inhibiting effects on proliferation of pancreatic cancer cells than ATO in vitro. In bearing-tumor mice, PDTC-ATO inhibited tumor growth by 79%, being more potent than ATO (by 46%) or PDTC (by 35%) compared to the control. Results of Western blot and immunohistochemistry showed proteasome inhibition and apoptotic cell death, together with obvious suppression of associating E3 ubiquitin ligase activity, occurred more frequently in tumors treated with PDTC-ATO than those with ATO.
conclusionPDTC demonstrated the function to facilitate ATO against pancreatic cancer due to forming a stable complex to perturb ubiquitin-proteasome pathway.
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Registered trials
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