ArticleMolecular and cellular biology2014
MicroRNAs 206 and 21 cooperate to promote RAS-extracellular signal-regulated kinase signaling by suppressing the translation of RASA1 and SPRED1.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- MicroRNA-mediated Krüppel-like factor 4 upregulation induces alternatively activated macrophage-associated marker and chemokine transcription in 4,4'-methylene diphenyl diisocyanate exposed macrophages.Xenobiotica; the fate of foreign compounds in biological systems · 2024Article
- Immune cell-derived extracellular vesicular microRNAs induce pancreatic beta cell apoptosis.Heliyon · 2022Article
- Nanotechnological Approaches for the Treatment of Triple-Negative Breast Cancer: A Comprehensive Review.Current drug metabolism · 2022Review
- Genetic susceptibility to acute graft versus host disease in pediatric patients undergoing HSCT.Bone marrow transplantation · 2021Article
- miR-188-5p promotes oxaliplatin resistance by targeting RASA1 in colon cancer cells.Oncology letters · 2021Article
- Review
- Role of RASA1 in cancer: A review and update (Review).Oncology reports · 2020Review
- Review
- Pumping the brakes on RAS - negative regulators and death effectors of RAS.Journal of cell science · 2020Review
- Acute 4,4'-Methylene Diphenyl Diisocyanate Exposure-Mediated Downregulation of miR-206-3p and miR-381-3p Activates Inducible Nitric Oxide Synthase Transcription by Targeting Calcineurin/NFAT Signaling in Macrophages.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Systems biology-based investigation of cooperating microRNAs as monotherapy or adjuvant therapy in cancer.Nucleic acids research · 2019Review
- MicroRNA‑4530 suppresses cell proliferation and induces apoptosis by targeting RASA1 in human umbilical vein endothelial cells.Molecular medicine reports · 2019Article
- MicroRNA regulation of K-Ras in pancreatic cancer and opportunities for therapeutic intervention.Seminars in cancer biology · 2019Review
- Circulating miRs-183-5p, -206-3p and -381-3p may serve as novel biomarkers for 4,4'-methylene diphenyl diisocyanate exposure.Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2019Article
- The "Yin and Yang" of Natural Compounds in Anticancer Therapy of Triple-Negative Breast Cancers.Cancers · 2018Review
- MiR-126 enhances VEGF expression in induced pluripotent stem cell-derived retinal neural stem cells by targeting spred-1.International journal of clinical and experimental pathology · 2018Article
- Co-expression and significance of Dok2 and Ras p21 protein activator 1 in breast cancer.Oncology letters · 2017Article
- Downregulation of CCL2 induced by the upregulation of microRNA-206 is associated with the severity of HEV71 encephalitis.Molecular medicine reports · 2017Article
- miR-148a and miR-17-5p synergistically regulate milk TAG synthesis via PPARGC1A and PPARA in goat mammary epithelial cells.RNA biology · 2017Article
- Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Despite the low prevalence of activating point mutation of RAS or RAF genes, the RAS-extracellular signal-regulated kinase (ERK) pathway is implicated in breast cancer pathogenesis. Indeed, in triple-negative breast cancer (TNBC), there is recurrent genetic alteration of pathway components. Using short hairpin RNA (shRNA) methods, we observed that the zinc finger transcription factor Krüppel-like factor 4 (KLF4) can promote RAS-ERK signaling in TNBC cells. Endogenous KLF4 bound to the promoter regions and promoted the expression of two microRNAs (miRs), miR-206 and miR-21 (i.e., miR-206/21). Antisense-mediated knockdown (anti-miR) revealed that miR-206/21 coordinately promote RAS-ERK signaling and the corresponding cell phenotypes by inhibiting translation of the pathway suppressors RASA1 and SPRED1. In TNBC cells, including cells with mutation of RAS, the suppression of either RASA1 or SPRED1 increased the levels of GTP-bound, wild-type RAS and activated ERK 1/2. Unlike the control cells, treatment of RASA1- or SPRED1-suppressed cells with anti-miR-206/21 had little or no impact on the level of activated ERK 1/2 or on cell proliferation and failed to suppress tumor initiation. These results identify RASA1 and SPRED1 mRNAs as latent RAS-ERK pathway suppressors that can be upregulated in tumor cells by anti-miR treatment. Consequently, KLF4-regulated miRs are important for the maintenance of RAS-ERK pathway activity in TNBC cells.
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Registered trials
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