Interleukin-6 dependent survival of multiple myeloma cells involves the Stat3-mediated induction of microRNA-21 through a highly conserved enhancer.
By D. Löffler, K. Brocke-Heidrich, G. Pfeifer, Claudia Stocsits, Jörg Hackermüller, A. Kretzschmar, R. Burger, M. Gramatzki, C. Blumert, K. Bauer and 4 more. Blood, 2007
681 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/1990e55bec93ea8105799ed5ace8c4679b1daa4d
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In Cancer Research
- Marilena V. Iorio
- Carlo Maria Croce
- T. Hirano
- Galina Gabriely
- D. Iliopoulos
- Anna M. Krichevsky
- Peter S. Linsley
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In Molecular Biology
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- D. Iliopoulos
- Carlo Maria Croce
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In Oncology
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Citations in the corpus
- MicroRNA 21 Promotes Glioma Invasion by Targeting Matrix Metalloproteinase Regulators (2008, background): “Interestingly, STAT3 can potentially mediate IL-6–miR-21 autocrine feedback.”
- STAT3 activation of miR-21 and miR-181b-1, via PTEN and CYLD, are part of the epigenetic switch linking inflammation to cancer (2010, background): “Although examples of transcription factors directly regulating microRNA expression have been described (O’Donnell et al., 2005; Löffler et al., 2007; Chang et al., 2008; Lin et al., 2009), microRNA promoters and transcription start sites were largely unknown until recently, thereby making it difficu”
- IL-6 in inflammation, autoimmunity and cancer (2020, background): “Furthermore, oncogenic miR-21 and miR-181b are targets of IL-6–STAT3, leading to the activation of NF-κ B (90, 141).”
- MicroRNAs in cancer: small molecules with a huge impact. (2009, background): “Few recent evidences have linked microRNAs to this plasma cell malignancy, as the aberrant expression of miR335, miR-342-3p, and miR-561 in comparison with normal plasma cells(47) or the Stat3-mediated activation of the oncogenic miR-21 in response to interleukin-6.(16) More recently, Pichiorri et a”
- MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “…to induce a metastatic phenotype Shown to inhibit apoptosis PTEN, TPM1 and PDCD4 Asangani et al. (2008); Chan et al. (2005); Frankel et al. (2007); Loffler et al. (2007); Meng et al. (2007a); Roldo et al. (2006); Si et al. (2007); Zhu et al. (2007) miR-29 Suggested to participate in maintaining…”
- Negative regulation of TLR4 via targeting of the proinflammatory tumor suppressor PDCD4 by the microRNA miR-21 (2010, methodology): “We found that the induction of miR-21 by LPS was dependent on MyD88 and also dependent on NF-κB, consistent with the presence of an NF-κB-binding site in the miR-21 promote”