NF-κB is essential for epithelial-mesenchymal transition and metastasis in a model of breast cancer progression
By M. Huber, N. Azoitei, B. Baumann, S. Grünert, A. Sommer, H. Pehamberger, N. Kraut, H. Beug, Thomas Wirth. 2004
777 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/27b68a766d216d3c3debe2d1c8e2c800f370e426
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- J. López-Novoa
- R. Huang
- M. Nieto
- J. P. Thiery
- Johannes A. Schmid
- Gregory J. Goodall
- Bastian Hoesel
- R. Hynes
In Molecular Biology
In Oncology
Citations in the corpus
- Vimentin as a potential molecular target in cancer therapy Or Vimentin, an overview and its potential as a molecular target for cancer therapy (2011, neutral): “It has been shown that NF-jB, a key protein regulating the immune and inflammatory process, also plays an important role in regulating the EMT process [48] and that its inhibition in mesenchymal cells can reverse the EMT process [ 49 ], suggesting that NF-jB is important in both activation and maint”
- The complexity of NF-κB signaling in inflammation and cancer (2013, background): “Moreover, NF-κB signaling was shown to contribute to cancer progression by controlling epithelial to mesenchymal transition and metastasis [84].”
- Direct Signaling Between Platelets and Cancer Cells Induces an Epithelial-Mesenchymal-Like Transition and Promotes Metastasis (2011, background): “NF-kB regulates the expression of proinflammatory genes and has been associated with increased metastasis and EMT induction (Huber et al., 2004; Lin and Karin, 2007).”
- The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1 (2008, background): “Several studies using in vivo mouse-model systems have suggested that EMT is involved in breast cancer metastasi”
- A cytoplasmic NF-κB interacting long noncoding RNA blocks IκB phosphorylation and suppresses breast cancer metastasis. (2015, background): “Further, a constitutively active IKKb (CA-IKK2) (Huber et al., 2004) in MDA-MB-231 cells induced NF-kB activation and upregulated NKILA expression, which could be completely inhibited by Sc-3060 or JSH-23 (Figure 1D).”
- Epithelial-mesenchymal transitions in development and disease. (2009, background): “The importance of this pathway is evidenced by the blocking of EMT elicited by nondestructible IkB, a NFκB inhibitor (Huber et al., 2004).”
- NF-κB represses E-cadherin expression and enhances epithelial to mesenchymal transition of mammary epithelial cells: potential involvement of ZEB-1 and ZEB-2 (2007, background): “Using these cells, Huber et al. (2004) showed the requirement of NF-kB in TGF-b1-induced EMT and metastasis.”