ArticleBlood2014
Targeting MUC1-C is synergistic with bortezomib in downregulating TIGAR and inducing ROS-mediated myeloma cell death.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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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.
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Who cites it
44 citing papers in PubMed, 66 citations in OpenAlex.
- Triptonide enhances DNA damage by inhibiting TRIP13‑mediated DNA repair and synergizes with bortezomib to suppress multiple myeloma.International journal of oncology · 2026Article
- Evolution of the MUC1 gene in eutherian mammals as an adaptation responsible for the increasing incidence of cancer in humans.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Enhanced anticancer effect of carfilzomib by codelivery of calcium peroxide nanoparticles targeting endoplasmic reticulum stress.Materials today. Bio · 2025Article
- Acquired Bortezomib Resistance in Multiple Myeloma: From Mechanisms to Strategy.Current treatment options in oncology · 2024Review
- Different Strategies to Overcome Resistance to Proteasome Inhibitors-A Summary 20 Years after Their Introduction.International journal of molecular sciences · 2024Review
- Article
- Redox-Responsive Polymeric Nanoparticle for Nucleic Acid Delivery and Cancer Therapy: Progress, Opportunities, and Challenges.Macromolecular bioscience · 2024Review
- Article
- Modulation of Cellular Redox Parameters for Improving Therapeutic Responses in Multiple Myeloma.Antioxidants (Basel, Switzerland) · 2022Review
- The role of TIGAR in nervous system diseases.Frontiers in aging neuroscience · 2022Review
- Contribution of the Tumor Microenvironment to Metabolic Changes Triggering Resistance of Multiple Myeloma to Proteasome Inhibitors.Frontiers in oncology · 2022Review
- Mucin 20 modulates proteasome capacity through c-Met signalling to increase carfilzomib sensitivity in mantle cell lymphoma.Journal of cellular and molecular medicine · 2021Article
- Mucin1 and Mucin16: Therapeutic Targets for Cancer Therapy.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Review
- siRNA-Inhibition of TIGAR Hypersensitizes Human Papillomavirus-Transformed Cells to Apoptosis Induced by Chemotherapy Drugs that Cause Oxidative Stress.Journal of antivirals & antiretrovirals · 2021Article
- Effect of bortezomib on proliferation and apoptosis of myeloma cells by activating Wnt/β-catenin signaling pathway.Oncology letters · 2020Article
- Redox Homeostasis and Metabolism in Cancer: A Complex Mechanism and Potential Targeted Therapeutics.International journal of molecular sciences · 2020Review
- The role of transporters in cancer redox homeostasis and cross-talk with nanomedicines.Asian journal of pharmaceutical sciences · 2020Review
- Pluronic block copolymers enhance the anti-myeloma activity of proteasome inhibitors.Journal of controlled release : official journal of the Controlled Release Society · 2019Article
- Inhibition of MUC1-C regulates metabolism by AKT pathway in esophageal squamous cell carcinoma.Journal of cellular physiology · 2019Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The proteosome inhibitor bortezomib (BTZ) induces endoplasmic reticulum and oxidative stress in multiple myeloma (MM) cells. The mucin 1 C-terminal subunit (MUC1-C) oncoprotein is aberrantly expressed in most MM cells, and targeting MUC1-C with GO-203, a cell-penetrating peptide inhibitor of MUC1-C homodimerization, is effective in inducing reactive oxygen species (ROS)-mediated MM cell death. The present results demonstrate that GO-203 and BTZ synergistically downregulate expression of the p53-inducible regulator of glycolysis and apoptosis (TIGAR), which promotes shunting of glucose-6-phosphate into the pentose phosphate pathway to generate reduced glutathione (GSH). In turn, GO-203 blocks BTZ-induced increases in GSH and results in synergistic increases in ROS and MM cell death. The results also demonstrate that GO-203 is effective against BTZ-resistant MM cells. We show that BTZ resistance is associated with BTZ-induced increases in TIGAR and GSH levels, and that GO-203 resensitizes BTZ-resistant cells to BTZ treatment by synergistically downregulating TIGAR and GSH. The GO-203/BTZ combination is thus highly effective in killing BTZ-resistant MM cells. These findings support a model in which targeting MUC1-C is synergistic with BTZ in suppressing TIGAR-mediated regulation of ROS levels and provide an experimental rationale for combining GO-203 with BTZ in certain settings of BTZ resistance.
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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.