ArticleMolecular and cellular biology2016
Suppression of MicroRNA 200 Family Expression by Oncogenic KRAS Activation Promotes Cell Survival and Epithelial-Mesenchymal Transition in KRAS-Driven Cancer.
Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- miRNAs, Mesenchymal Stromal Cells and Major Neoplastic and Inflammatory Skin Diseases: A Page Being Written: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Restoration of miR-200 expression suppresses proliferation and mobility of pancreatic cancer cell.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Role and mechanism of IGFBP5 in the real-ambient particulate matter exposure-induced chronic lung injury.Frontiers in pharmacology · 2025Article
- miR-200b-3p relieved inflammation in patients with heart failure by regulating ZEB1 expression.Journal of cardiothoracic surgery · 2024Article
- Cooperative pro-tumorigenic adaptation to oncogenic RAS through epithelial-to-mesenchymal plasticity.Science advances · 2024Article
- The miR-143/145 cluster induced by TGF-β1 suppresses Wilms' tumor 1 expression in cultured human podocytes.American journal of physiology. Renal physiology · 2023Article
- Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023Review
- Role of miR‑200 family in brain metastases: A systematic review.Molecular and clinical oncology · 2023Article
- Molecular characterization of colorectal cancer related peritoneal metastatic disease.Nature communications · 2022Article
- Crucial Role of OncogenicCells · 2022Review
- Interplay between K-RAS and miRNAs.Trends in cancer · 2022Review
- Regulation of ZEB1 Function and Molecular Associations in Tumor Progression and Metastasis.Cancers · 2022Review
- The miR-200 Family of microRNAs: Fine Tuners of Epithelial-Mesenchymal Transition and Circulating Cancer Biomarkers.Cancers · 2021Review
- MYSM1 inhibits human colorectal cancer tumorigenesis by activating miR-200 family members/CDH1 and blocking PI3K/AKT signaling.Journal of experimental & clinical cancer research : CR · 2021Article
- NEM-Tar: A Probabilistic Graphical Model for Cancer Regulatory Network Inference and Prioritization of Potential Therapeutic Targets From Multi-Omics Data.Frontiers in genetics · 2021Article
- Article
- The Non-Coding Landscape of Cutaneous Malignant Melanoma: A Possible Route to Efficient Targeted Therapy.Cancers · 2020Review
- Tranilast induces MiR-200c expression through blockade of RelA/p65 activity in leiomyoma smooth muscle cells.Fertility and sterility · 2020Article
- Extracellular Vesicles and Epigenetic Modifications Are Hallmarks of Melanoma Progression.International journal of molecular sciences · 2019Review
- Nonsense-mediated mRNA decay: The challenge of telling right from wrong in a complex transcriptome.Wiley interdisciplinary reviews. RNA · 2019Review
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
Oncogenic KRAS contributes to malignant transformation, antiapoptosis, and metastasis in multiple human cancers, such as lung, colon, and pancreatic cancers and melanoma. MicroRNAs (miRNAs) are endogenous 18- to 25-nucleotide noncoding small RNAs that regulate gene expression in a sequence-specific manner via the degradation of target mRNAs or inhibition of protein translation. In the present study, using array-based miRNA profiling in IMR90 and MCF10A cells expressing oncogenic KRAS, we identified that the expression of the microRNA 200 (mir-200) family was suppressed by KRAS activation and that this suppression was mediated by the transcription factors JUN and SP1 in addition to ZEB1. Restoration of mir-200 expression compromised KRAS-induced cellular transformation in vitro and tumor formation in vivo In addition, we found that enforced expression of mir-200 abrogated KRAS-induced resistance to apoptosis by directly targeting the antiapoptotic gene BCL2 Finally, mir-200 was able to antagonize the epithelial-mesenchymal transition (EMT) driven by mutant KRAS. Collectively, our results suggest that repression of endogenous mir-200 expression is one of the important cellular responses to KRAS activation during tumor initiation and progression.
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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.