ArticlePloS one2012
Forced expression of miR-143 represses ERK5/c-Myc and p68/p72 signaling in concert with miR-145 in gut tumors of Apc(Min) mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 45 citations in OpenAlex.
- Berberine Attenuates Hypertrophic Phenotype in RAF1-Mutant Induced Pluripotent Stem Cell-Derived Cardiomyocytes through Suppression of ERK5-Cyclin D1 Signaling.Cardiovascular drugs and therapy · 2026Article
- Bone and Extracellular Signal-Related Kinase 5 (ERK5).Biomolecules · 2024Review
- MicroRNAs and 'Sponging' Competitive Endogenous RNAs Dysregulated in Colorectal Cancer: Potential as Noninvasive Biomarkers and Therapeutic Targets.International journal of molecular sciences · 2022Review
- Short-Chain Fatty Acid Decreases the Expression of CEBPB to Inhibit miR-145-Mediated DUSP6 and Thus Further Suppresses Intestinal Inflammation.Inflammation · 2022Article
- The Role of PKM2 in Metabolic Reprogramming: Insights into the Regulatory Roles of Non-Coding RNAs.International journal of molecular sciences · 2021Review
- Review
- Intercalating the Role of MicroRNAs in Cancer: As Enemy or Protector.Asian Pacific journal of cancer prevention : APJCP · 2020Review
- MicroRNA-145 targets in cancer and the cardiovascular system: evidence for common signaling pathways.Vascular biology (Bristol, England) · 2020Review
- Forced expression of miR-143 and -145 in cardiomyocytes induces cardiomyopathy with a reductive redox shift.Cellular & molecular biology letters · 2020Article
- Diagnostic value of a microRNA signature panel in exosomes for patients with hepatocellular carcinoma.International journal of clinical and experimental pathology · 2019Article
- Function of microRNA-145 and mechanisms underlying its role in malignant tumor diagnosis and treatment.Cancer management and research · 2019Review
- Cardamonin reduces chemotherapy resistance of colon cancer cells via the TSP50/NF-κB pathwayOncology letters · 2018Article
- Impairment of K-Ras signaling networks and increased efficacy of epidermal growth factor receptor inhibitors by a novel synthetic miR-143.Cancer science · 2018Article
- Potential relevance of microRNAs in inter-species epigenetic communication, and implications for disease pathogenesis.RNA biology · 2017Review
- miR-143 is associated with proliferation and apoptosis involving ERK5 in HeLa cells.Oncology letters · 2016Article
- ERK5 signalling rescues intestinal epithelial turnover and tumour cell proliferation upon ERK1/2 abrogation.Nature communications · 2016Article
- A novel IL-17 signaling pathway controlling keratinocyte proliferation and tumorigenesis via the TRAF4-ERK5 axis.The Journal of experimental medicine · 2015Article
- A novel chemopreventive strategy based on therapeutic microRNAs produced in plants.Cell research · 2015Article
- P68 RNA helicase as a molecular target for cancer therapy.Journal of experimental & clinical cancer research : CR · 2014Review
- Extracellular disposal of tumor-suppressor miRs-145 and -34a via microvesicles and 5-FU resistance of human colon cancer cells.International journal of molecular sciences · 2014Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, miR-143 and miR-145 have been shown to belong to a subset of microRNAs whose expression is controlled by a complex of a tumor suppressor p53 and DEAD-box RNA helicase subunits p68/p72. While accumulating studies have acknowledged that both miRNAs function as tumor suppressors and are similarly regulated, evidence of their coordinated action against tumorigenesis has been poorly presented. Herein, we establish transgenic mice that express miR-143 under the control of the CAG regulatory unit. When crossbred with Apc(Min/+) mice, the development of tumors in the small intestines is significantly attenuated. In the transgenic small intestine tumors, the endogenous miR-145 is also enhanced and the expression of c-Myc and p68/p72, both of which have been reported to be pivotal for gut tumor development, is suppressed, corresponding to the downregulation of ERK5. We demonstrate that the combination of miR-143 and miR-145 inhibits the expression of c-Myc in human colon cancer cells, whereas miR-145 retards that of p72. Moreover, we show the possibilities that miR-145 modulates p72 expression through its 3' untranslated region and that c-Myc downregulation is involved in both p68 suppression and miR-145 induction. These findings suggest that forced expression of miR-143, probably interacting with endogenous miR-145, inhibits ERK5/c-Myc and p68/p72/β-catenin signaling and hampers small intestine tumor development in Apc(Min/+) mice. This unique cascade, in turn, may prevent overproduction of a subset of tumor suppressive miRNAs by repressing their own modulators, p68/p72.
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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.