gp130-mediated Stat3 activation in enterocytes regulates cell survival and cell-cycle progression during colitis-associated tumorigenesis.

By J. Bollrath, T. Phesse, Vivian A. von Burstin, Tracy L. Putoczki, Moritz Bennecke, Trudie Bateman, Tim Nebelsiek, Therese Lundgren-May, Ozge Canli, S. Schwitalla and 6 more. Cancer Cell, 2009

993 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology, Surgery

View Paper: https://www.semanticscholar.org/paper/0daaf15efdce149472e898216991b9b42470a7ae

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Citations in the corpus

STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing (2009, result): “Our data are also consistent with two very recently published studies in which IL-6/gp130mediated STAT3 activation during tumor development was shown to drive cell proliferation of enterocytes (Bollrath et al., 2009; Grivennikov et al., 2009).”
Cancer-related inflammation: common themes and therapeutic opportunities. (2012, background): “IL-6 also has tumor-promoting actions on both malignant and stromal cells in a range of experimental cancer models [43–45], is a downstream effector of oncogenic ras [46] and has been implicated in several human cancers including multiple myeloma [47] and hepatocellular carcinoma [48].”
IL-6 and STAT3 are required for survival of intestinal epithelial cells and development of colitis associated cancer (2009, background): “Similarly, gp130 mutations that prevent SOCS3 binding lead to Stat3 hyperactivation and spon-taneous gastrointestinal tumorigenesis (Ernst et al., 2008; Jenkins et al., 2005; Judd et al., 2004; Bollrath et al., 2009).”
Stat3/Socs3 activation by IL-6 transsignaling promotes progression of pancreatic intraepithelial neoplasia and development of pancreatic cancer. (2011, background): “associated colorectal carcinogenesis, for example, myeloid IL-6 activates Stat3 to promote the formation of adenoma and tumors (Bollrath et al., 2009; Grivennikov et al., 2009).”
Experimental adaptation of an influenza H5 haemagglutinin (HA) confers respiratory droplet transmission to a reassortant H5 HA/H1N1 virus in ferrets (2012, neutral): “6 (3) 5 of 5 (40, 20, 20, 40, 40) 0 of 5 0 of 5 (,10, ,10, ,10, ,10, ,10)”
Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer (2009, background): “Indeed, we and others found that inactivation of STAT3 in epithelial cells not only reduces tumorigenicity in a mouse model of CAC, but more specifically, attenuates the expression of the anti-apoptotic protein Bcl-XL, as well as other pro-survival and tissue protective proteins and cell cycle regul”
IL-6R/STAT3/miR-34a feedback loop promotes EMT-mediated colorectal cancer invasion and metastasis. (2014, background): “Since miR-34a was expressed at more than approximately 1000-fold higher levels than miR-34b and miR-34c in intestinal epithelia and approximately 180-fold higher in intestinal tumors (data not shown), we focused on the role of miR-34a in CAC.”
Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability. (2009, background): “IL-6 protects normal and premalignant intestinal epithelial cells from apoptosis and promotes the proliferation of tumor-initiating cells [30,31].”