ArticleOncogene2013
RREB1 repressed miR-143/145 modulates KRAS signaling through downregulation of multiple targets.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
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Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.
- Non-coding RNAs in exercise immunology: A systematic review.Journal of sport and health science · 2024Pooled it
- Epigenomic characterization of locally advanced anal cancer: a radiation therapy oncology group 98-11 specimen study.Diseases of the colon and rectum · 2014Trial
- Crosstalk between KRAS and miRNAs in pancreatic cancer: Opportunities for its diagnosis, prognosis and therapeutic intervention (Review).International journal of oncology · 2026Review
- The miR-143/145 cluster in prostate cancer: molecular regulation, context-dependent functions, and medical implications.Biology direct · 2026Review
- Review
- Tumor microenvironment-driven microRNA dysregulation: Key interactions in colorectal cancer progression.World journal of gastrointestinal oncology · 2026Review
- The multifaceted role of microRNAs in colorectal cancer: pathogenesis and therapeutic implications.Non-coding RNA research · 2025Review
- Role of Carvedilol in Inhibiting the Proliferation and Migration of Vascular Smooth Muscle Cells by Upregulating microRNA-145 Expression.Physiological research · 2025Article
- Identification of a Distal Enhancer That Regulates TGF-β-Induced SNAI1 Expression.Cancer science · 2025Article
- Plasma miR-145-5p Levels and Risk of Future Cancer-Results from the HUNT Study.International journal of molecular sciences · 2025Article
- Dynamic Coupling of MAPK Signaling to the Guanine Nucleotide Exchange Factor GEF-H1.OncoTargets and therapy · 2025Review
- RREB1-mediated SUMOylation enhancement promotes chemoresistance partially by transcriptionally upregulatingFrontiers in pharmacology · 2024Article
- Modeling methamphetamine use disorder and relapse in animals: short- and long-term epigenetic, transcriptional., and biochemical consequences in the rat brain.Neuroscience and biobehavioral reviews · 2023Review
- Novel insights on perils and promises of miRNA in understanding colon cancer metastasis and progression.Medical oncology (Northwood, London, England) · 2023Review
- miR-125b-5p, miR-155-3p, and miR-214-5p and TargetInternational journal of molecular sciences · 2023Article
- MicroRNAs in cancer metastasis: biological and therapeutic implications.Expert reviews in molecular medicine · 2023Review
- TGF-β in developmental and fibrogenic EMTs.Seminars in cancer biology · 2022Review
- Promotion or remission: a role of noncoding RNAs in colorectal cancer resistance to anti-EGFR therapy.Cell communication and signaling : CCS · 2022Review
- Article
- Blockade of the pro-fibrotic reaction mediated by the miR-143/-145 cluster enhances the responses to targeted therapy in melanoma.EMBO molecular medicine · 2022Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
A lack of expression of miR-143 and miR-145 has been demonstrated to be a frequent feature of colorectal tumors. Activating KRAS mutations have been reported in 30-60% of colorectal cancers and an inverse correlation between Kras and miR-143/145 expression has been observed. Previously, we have demonstrated that oncogenic Kras leads to repression of the miR-143/145 cluster in pancreatic cancer and is dependent on the Ras responsive element (RRE) binding protein (RREB1), which negatively regulates miR-143/145 expression. In the present study, we have found that RREB1 is overexpressed in colorectal adenocarcinoma tumors and cell lines, and the expression of the miR-143/145 primary transcript is inversely related to RREB1 expression. In colorectal cancer cell lines, the miR-143/145 cluster is repressed by RREB1 downstream of constitutively active KRAS. RREB1 is activated by the MAPK pathway and negatively represses the miR-143/145 promoter through interaction with two RREs. In addition, overexpression of miR-143 or miR-145 in HCT116 cells abrogates signaling through the MAPK, PI3K and JNK pathways by downregulation of both KRAS and RREB1 in addition to downregulation of a cohort of genes in the MAPK signaling cascade. These results establish a complex network of regulation through which the miR-143/145 cluster is able to modulate KRAS signaling in colorectal cancer.
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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.