TGF-β Suppresses Tumor Progression in Colon Cancer by Inhibition of IL-6 trans-Signaling

By C. Becker, M. Fantini, C. Schramm, H. Lehr, S. Wirtz, A. Nikolaev, J. Burg, Susanne Strand, R. Kiesslich, S. Huber and 8 more. 2004

676 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/72fc64594049af00a444125ae976440b88e761a3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. E. Batlle
2. M. Karin
3. S. Grivennikov
4. T. Lawrence
5. X. Zhang
6. Sivakumar Vallabhapurapu
7. C. Nadal
8. F. Greten

In Oncology

1. M. Karin
2. S. Grivennikov
3. S. Rose‐John
4. F. Greten
5. Markus F. Neurath
6. J. Massagué
7. T. Lawrence
8. E. Batlle

In Pathology and Forensic Medicine

1. M. Karin
2. S. Rose‐John
3. J. Massagué
4. S. Shalapour

Citations in the corpus

• Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer (2009, background): “NFkB induced IL-6, IL-1 and TNF-a have been implicated in tumor development and growth in several models, primarily by their ability to increase the survival and growth of cancer cells, but also through their effects on the immune system, which sustain tumorassociated inflammation [45,86,104,105].”
• NF-κB: linking inflammation and immunity to cancer development and progression (2005, background): “One of these factors seems to be IL-6, because injection of neutralizing antibodies that are specific for the IL-6 receptor also decreased tumour number and size in the CAC mode”
• STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing (2009, methodology): “Western blotting was performed as previously described (Becker et al., 2004).”
• gp130-mediated Stat3 activation in enterocytes regulates cell survival and cell-cycle progression during colitis-associated tumorigenesis. (2009, background): “…than IL-6 signaling, promotes tumorigenesis in a model of inflammationassociated gastric cancer (Ernst et al., 2008), while IL-6 has been proposed to play this role in the CAC model (Becker et al., 2004; see also the accompanying paper by Grivennikov et al. [2009] in this issue of Cancer Cell).”
• Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. (2006, background): “…of IL-6, whose expression is negatively regulated by IL-10, has yet to be examined in the IL-10 / mouse model of colorectal cancer; however, it should be noted that inhibition of IL-6 signaling retards development of chemically induced colitisassociated cancer (CAC) in mice (Becker et al., 2004).”
• A cytokine-mediated link between innate immunity, inflammation, and cancer. (2007, neutral): “TGF-β signaling prevents the release of IL-6 from Th1 cells during the late stages of CAC and therefore functions to control tumor growth (66).”