ArticleBritish journal of haematology2017
MUC1-C is a target in lenalidomide resistant multiple myeloma.
Article in British journal of haematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Advances in adoptive cellular immunotherapy and therapeutic breakthroughs in multiple myeloma.Experimental hematology & oncology · 2024Review
- Preclinical and clinical evaluation of the Janus Kinase inhibitor ruxolitinib in multiple myeloma.Oncotarget · 2024Article
- The multifaceted role of MUC1 in tumor therapy resistance.Clinical and experimental medicine · 2023Review
- Novel insights into the roles and therapeutic implications of MUC1 oncoprotein via regulating proteins and non-coding RNAs in cancer.Theranostics · 2022Review
- Mucin1 and Mucin16: Therapeutic Targets for Cancer Therapy.Pharmaceuticals (Basel, Switzerland) · 2021Review
- The role of Wnt/β-catenin signaling pathway in the pathogenesis and treatment of multiple myeloma (review).American journal of translational research · 2021Review
- Matrix Metalloprotease-7 Mediates Nucleolar Assembly and Intra-nucleolar Cleaving p53 in Gefitinib-Resistant Cancer Stem Cells.iScience · 2020Article
- High-Risk Multiple Myeloma: Integrated Clinical and Omics Approach Dissects the Neoplastic Clone and the Tumor Microenvironment.Journal of clinical medicine · 2019Review
- Inhibition of MUC1-C regulates metabolism by AKT pathway in esophageal squamous cell carcinoma.Journal of cellular physiology · 2019Article
- Inhibition of MUC1-C entering nuclear suppresses MYC expression and attenuates malignant growth in esophageal squamous cell carcinoma.OncoTargets and therapy · 2018Article
- Multiple Roles of Glycans in Hematological Malignancies.Frontiers in oncology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Lenalidomide (LEN) acts directly on multiple myeloma (MM) cells by inducing cereblon-mediated degradation of interferon regulatory factor 4, Ikaros (IKZF)1 and IKZF3, transcription factors that are essential for MM cell survival. The mucin 1 (MUC1) C-terminal transmembrane subunit (MUC1-C) oncoprotein is aberrantly expressed by MM cells and protects against reactive oxygen species (ROS)-mediated MM cell death. The present studies demonstrate that targeting MUC1-C with GO-203, a cell-penetrating peptide inhibitor of MUC1-C homodimerization, is more than additive with LEN in downregulating the WNT/β-catenin pathway, suppressing MYC, and inducing late apoptosis/necrosis. We show that the GO-203/LEN combination acts by synergistically increasing ROS and, in turn, suppressing β-catenin. LEN resistance has been linked to activation of the WNT/β-catenin→CD44 pathway. In this regard, our results further demonstrate that targeting MUC1-C is effective against LEN-resistant MM cells. Moreover, GO-203 resensitized LEN-resistant MM cells to LEN treatment in association with suppression of β-catenin and CD44. Targeting MUC1-C also resulted in downregulation of CD44 on the surface of primary MM cells. These findings, and the demonstration that expression of MUC1 and CD44 significantly correlate in microarrays from primary MM cells, provide support for combining GO-203 with LEN in the treatment of MM and in LEN-resistance.
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Registered trials
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