ArticleOncotarget2016
MiRNA-29a as a tumor suppressor mediates PRIMA-1Met-induced anti-myeloma activity by targeting c-Myc.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Degradation of MYC by the mutant p53 reactivator drug, COTI-2 in breast cancer cells.Investigational new drugs · 2023Article
- Review
- The Role of Non-Coding RNAs in the Regulation of the Proto-Oncogene MYC in Different Types of Cancer.Biomedicines · 2021Review
- Review
- Potential Role of microRNAs in inducing Drug Resistance in Patients with Multiple Myeloma.Cells · 2021Review
- Antitumor Effects of PRIMA-1 and PRIMA-1Cells · 2021Review
- Synergistic effects of PRIMA-1Haematologica · 2020Article
- Ectopic expression of BIRC5-targeting miR-101-3p overcomes bone marrow stroma-mediated drug resistance in multiple myeloma cells.BMC cancer · 2019Article
- MicroRNA-765 is pregulated in multiple myeloma and serves an oncogenic role by directly targeting SOX6.Experimental and therapeutic medicine · 2019Article
- Factors Regulating microRNA Expression and Function in Multiple Myeloma.Non-coding RNA · 2019Review
- MicroRNAs and cholangiocarcinoma: elucidating the effects of tiny giants.AME medical journal · 2018Article
- The potential function of microRNAs as biomarkers and therapeutic targets in multiple myeloma.Oncology letters · 2018Review
- MicroRNA-29a Functions as a Tumor Suppressor and Increases Cisplatin Sensitivity by Targeting NRAS in Lung Cancer.Technology in cancer research & treatment · 2018Article
- PRIMA-1 and PRIMA-1Cancers · 2017Review
- Aspirin regulation of c-myc and cyclinD1 proteins to overcome tamoxifen resistance in estrogen receptor-positive breast cancer cells.Oncotarget · 2017Article
- Inhibiting the system xNature communications · 2017Article
- Role of micro-RNAs in drug resistance of multiple myeloma.Oncotarget · 2016Review
- Review
- MicroRNA-based screens for synthetic lethal interactions with c-Myc.RNA & disease (Houston, Tex.) · 2016Article
- MicroRNA-497 suppresses cell proliferation and induces apoptosis through targeting PBX3 in human multiple myeloma.American journal of cancer research · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proto-oncogene c-Myc plays substantial role in multiple myeloma (MM) pathogenesis and is considered a potential drug target. Here we provide evidence of a novel mechanism for PRIMA-1Met, a small molecule with anti-tumor activity in phase I/II clinical trial, showing that PRIMA-1Met induces apoptosis in MM cells by suppressing c-Myc and upregulating miRNA-29a. Our study further demonstrates that miRNA-29a functions as a tumor suppressor which targets c-Myc. The baseline expression of miR-29a was significantly lower in MM cell lines and MM patient samples compared to normal hematopoietic cells. In addition, ectopic expression of miRNA-29a or exposure to PRIMA-1Met reduced cell proliferation and induced apoptosis in MM cells. On the other hand, overexpression of c-Myc at least partially reverted the inhibitory effects of PRIMA-1Met or miRNA-29a overexpression suggesting the miRNA-29a/c-Myc axis mediates anti-myeloma effects of PRIMA-1Met. Importantly, intratumor delivery of miRNA-29a mimics induced regression of tumors in mouse xenograft model of MM and this effect synergized with PRIMA-1Met. Our study indicates that miRNA-29a is a tumor suppressor that plays an important role during PRIMA-1Met-induced apoptotic signaling by targeting c-Myc and provides the basis for novel therapeutic strategies using miRNA-29a mimics combined with PRIMA-1Met in MM.
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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.