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000127516 0247_ $$2doi$$a10.1016/j.molonc.2015.01.008
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000127516 1001_ $$0P:(DE-HGF)0$$aShukla, Kirti$$b0$$eFirst author
000127516 245__ $$aMicroRNA-30c-2-3p negatively regulates NF-κB signaling and cell cycle progression through downregulation of TRADD and CCNE1 in breast cancer.
000127516 260__ $$aAmsterdam [u.a.]$$bElsevier$$c2015
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000127516 520__ $$aNuclear Factor kappa B (NF-κB) signaling is frequently deregulated in a variety of cancers and is constitutively active in estrogen receptor negative (ER-) breast cancer subtypes. These molecular subtypes of breast cancer are associated with poor overall survival. We focused on mechanisms of NF-κB regulation by microRNAs (miRNAs), which regulate eukaryotic gene expression at the post-transcriptional level. In a previous genome-wide miRNA screen, we had identified miR-30c-2-3p as one of the strongest negative regulators of NF-κB signaling. Here we have uncovered the underlying molecular mechanisms and its consequences in breast cancer. In vitro results show that miR-30c-2-3p directly targets both TNFRSF1A-associated via death domain (TRADD), an adaptor protein of the TNFR/NF-κB signaling pathway, and the cell cycle protein Cyclin E1 (CCNE1). Ectopic expression of miR-30c-2-3p downregulated essential cytokines IL8, IL6, CXCL1, and reduced cell proliferation as well as invasion in MDA-MB-231 breast cancer cells. RNA interference (RNAi) induced silencing of TRADD phenocopied the effects on invasion and cytokine expression caused by miR-30c-2-3p, while inhibition of CCNE1 phenocopied the effects on cell proliferation. We further confirmed the tumor suppressive role of this miRNA using a dataset of 781 breast tumors, where higher expression was associated with better survival in breast cancer patients. In summary we have elucidated the mechanism by which miR-30c-2-3p negatively regulates NF-κB signaling and cell cycle progression in breast cancer.
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000127516 650_7 $$2NLM Chemicals$$aCCNE1 protein, human
000127516 650_7 $$2NLM Chemicals$$aCyclin E
000127516 650_7 $$2NLM Chemicals$$aMIRN30 microRNA, human
000127516 650_7 $$2NLM Chemicals$$aMicroRNAs
000127516 650_7 $$2NLM Chemicals$$aNF-kappa B
000127516 650_7 $$2NLM Chemicals$$aOncogene Proteins
000127516 650_7 $$2NLM Chemicals$$aRNA, Neoplasm
000127516 650_7 $$2NLM Chemicals$$aTNF Receptor-Associated Death Domain Protein
000127516 7001_ $$0P:(DE-He78)ef6b064b6d3463cee768ed2e261c10cd$$aSharma, Ashwini Kumar$$b1$$udkfz
000127516 7001_ $$0P:(DE-HGF)0$$aWard, Aoife$$b2
000127516 7001_ $$0P:(DE-He78)18218139eec55d83cf82679934e5cd75$$aWill, Rainer$$b3$$udkfz
000127516 7001_ $$0P:(DE-He78)743a4a82daab55306a2c88b9f6bf8c2f$$aHielscher, Thomas$$b4$$udkfz
000127516 7001_ $$0P:(DE-HGF)0$$aBalwierz, Aleksandra$$b5
000127516 7001_ $$0P:(DE-He78)cfaf278e8f522c72644cee2a753d2845$$aBreunig, Christian$$b6$$udkfz
000127516 7001_ $$0P:(DE-He78)610dc3a15bda751de4d4c52373b2620f$$aMünstermann, Ewald$$b7$$udkfz
000127516 7001_ $$0P:(DE-He78)4291b9a1fa95bfd7a810372e2d629c32$$aKönig, Rainer$$b8$$udkfz
000127516 7001_ $$0P:(DE-HGF)0$$aKeklikoglou, Ioanna$$b9
000127516 7001_ $$0P:(DE-He78)f6bebe05e7a748d3cbf9f59659567d52$$aWiemann, Stefan$$b10$$eLast author$$udkfz
000127516 773__ $$0PERI:(DE-600)2322586-5$$a10.1016/j.molonc.2015.01.008$$gVol. 9, no. 6, p. 1106 - 1119$$n6$$p1106 - 1119$$tMolecular oncology$$v9$$x1574-7891$$y2015
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